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Sir William Dunn School of Pathology, University of Oxford, Oxford, United Kingdom
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Previous work in this laboratory has demonstrated that a subset of
CD4+ T cells exists in normal
PVG.RT1u rats that is capable of preventing the
onset of IDDM that otherwise develops in syngeneic recipient rats with
experimentally induced lymphopenia (TxX rats) (2).
Fractionation of CD4+ T cells according to
expression of CD45RC revealed that the regulatory T cells were
contained in the CD45RClow fraction, which is the
phenotype associated with resting memory cells. The full phenotype of
these protective cells was
CD4+TCR
ß+CD45RClowRT6+Thy1-
(2). Despite the fact that according to their surface
phenotype the regulatory cells were Ag experienced, the thymus was also
found to contain a potent source of regulatory cells among the mature
CD4+CD8- subset (2, 3). Later experiments demonstrated that these intrathymic
regulatory cells had differentiated in situ rather than homed back to
the thymus from the periphery (4).
More recently, CD25 has emerged as a marker for T cells with regulatory
activity in mouse models of autoimmune gastritis. This autoimmune
disease, among others, develops in BALB/c mice rendered lymphopenic by
thymectomy at 3 days of age (5) or in nude recipients of
CD25- T cells (5, 6). In both models transfer
of a minority population of CD4+ T cells
expressing CD25 prevented autoimmune disease. The majority of these
CD25+ cells were CD45RBlow
(equivalent to CD45RClow cells in rats), and
hence corresponded to a subset of the regulatory cells previously
described in this laboratory. CD25 (IL-2R) expression is induced on
T cell activation to form part of the trimeric, high affinity IL-2R
complex in combination with CD122 (IL-2Rß) and CD132 (IL-2R
) and
has commonly been used as a marker for activated T cells. However, it
was reported that the majority of CD25+ T cells
in mice lacked coexpression of IL-2Rß ex vivo and were anergic in
vitro, as shown by nonproliferation to antigenic stimulation except in
the presence of high levels of exogenous IL-2 (7, 8, 9).
Thus, unlike activated cells, these regulatory cells may be expressing
homodimers of CD25, which have been reported to bind IL-2 with low
affinity and lack signaling capacity (10).
The observation in the mouse that the T cells that prevent organ-specific autoimmunity are CD25+ appeared to be contrary to earlier work from this laboratory, which established that at least some regulatory cells in the rat are CD25- (2). To further explore this apparent discrepancy in the data from the two species, work has been conducted on the phenotype of regulatory T cells in rats. The findings form the subject of this report.
Consistent with the published studies of T cells that prevent autoimmune gastritis in mice, we have now shown that CD25 is a phenotypic marker for CD4+ T cells in the thymus and peripheral lymphoid tissues of normal rats that prevent autoimmune diabetes. However, we have also shown that, compatible with earlier data in the rat, there is a population of peripheral CD4+CD45RC-CD25- T cells that can prevent diabetes. The protective activity of these cells from spleen and lymph nodes is revealed only after the removal of recent thymic emigrants (RTE) from this subset, suggesting the presence of diabetogenic cells in CD25- RTE that are insufficiently controlled by CD25- regulatory cells alone. Given that CD25 is expressed on both activated T cells as well as some regulatory T cells, and that, as we show here, not all regulatory T cells express CD25, it is evident that currently there is no marker that uniquely defines T cells that prevent organ-specific autoimmunity. Nevertheless, CD25 appears to be a useful marker for cells with regulatory activity in the thymus.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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The following mouse IgG1 Abs were tissue culture supernatants
produced from hybridomas in the Medical Research Council Cellular
Immunology Unit (Oxford, U.K.) by Mike Puklavec: OX8 (anti-rat
CD8) (11), OX22 (anti-rat CD45RC) (12, 13), OX32 (anti-rat CD45RC, noncompetitive with OX22)
(13, 14), OX39 (anti-rat CD25) (15),
NDS62 (anti-rat CD25, noncompetitive with OX39) (16),
W3/25 (anti-rat CD4) (17), OX21 (isotype control mouse
IgG1, reactive with human factor I) (18), OKT4
(anti-human CD4) (19), and OKT8 (anti-human CD8)
(20). Some of these Abs were purified and biotinylated
using standard methods.
Abs and fluorescent reagents obtained from commercial sources include W3/25-FITC, anti-human CD25-FITC, anti-human CD8-PECy5, and conjugated isotype control mAbs (all obtained from Serotec, Oxford, U.K.). Donkey anti-mouse IgG (DAM)-PE (Chemicon, Temecula, CA) was used to detect staining of the unconjugated mouse mAbs, and streptavidin-QR (Sigma, St. Louis, MO) was used to detect staining of biotinylated Abs.
Flow cytometry
For flow cytometric analysis, typically 106 cells were stained with 50 µl of the appropriately diluted Ab for 30 min on ice, washed twice with PBS/0.2% BSA, and analyzed on the FACScan (Becton Dickinson, Mountain View, CA). For triple-color analysis, cells were incubated first with the unconjugated mAb and washed, followed by detection with DAM-PE. After 20-min incubation with 5% normal mouse serum in PBS, the cells were coincubated with the FITC and biotin-conjugated Abs, washed, and incubated for an additional 30 min with streptavidin-QR.
Induction and monitoring of IDDM in PVG.RT1u rats
PVG.RT1u rats were bred and housed in specific pathogen-free conditions at the Sir William Dunn School of Pathology (Oxford, U.K.). IDDM was induced in female PVG.RT1u rats by a protocol involving thymectomy at 6 wk of age, followed by four doses of 250 rad gamma irradiation at 2-wk intervals, beginning 2 wk after thymectomy. This protocol was described in more detail previously (2, 21). Cells to be tested for regulatory activity were injected i.v. immediately following the last irradiation. Animals were subsequently weighed twice weekly for 12–15 wk, and those exhibiting weight loss were tested for the development of diabetes, as assessed by measurement of blood glucose levels using Glucostix (Bayer Diagnostics, Newburg, OK), and confirmed by the presence of glycosuria with Clinistix (Bayer Diagnostics). Animals were considered diabetic if their blood glucose levels were >16 mM and they also tested positive for glycosuria.
Purification of peripheral T cell subsets
Donor cells were obtained from pooled single-cell suspensions of cervical and mesenteric lymph nodes and spleen (after lysis of RBCs) or from the thoracic duct lymph (TDL) of 8- to 16-wk-old female PVG.RT1u rats. Cells from TDL were obtained by cannulation of the thoracic duct (22) and were collected at 4°C overnight into PBS containing heparin (2 U/ml final concentration). Enrichment for CD4+CD45RC- cells involved incubation for 50 min on ice with the mouse mAbs OX8, OX22, and OX32, followed by washing and two or three consecutive rounds of depletion with goat anti-mouse IgG-coated magnetic beads (Dynal, Oslo, Norway). At this stage, the efficiency of the depletion was tested by labeling cells pre- and postdepletion with DAM-PE for 20 min for flow cytometric analysis. The percentage of contaminating cells was consistently <5%. Fractionation of the enriched CD4+CD45RC- cells according to expression of CD25 was then performed by incubation of cells for 50 min on ice with OX39 and NDS62 (noncompeting Abs to CD25), followed by two washes, incubation with anti-mouse IgG-coated magnetic beads (Miltenyi Biotec, Auburn, CA), a further wash, and separation on a LS+ column (Miltenyi Biotec) according to the manufacturer’s instructions. The purity of the fractionated cells was again analyzed on the FACScan by labeling pre- and postdepletion samples with DAM-PE. The percentage of CD4+ cells in the fractionated cells was also determined by analysis on the FACScan after incubation of cells for 20 min with W3/25-FITC. It may be noted that although in principle the W3/25-FITC could be bound by the anti-mouse IgG-coated MACS beads on the surface of the positively selected cells, control experiments indicated that this potential problem did not detectably alter the pattern of staining (data not shown).
Purification of thymocyte subsets
Enrichment of CD4+CD8- thymocytes was performed by negative selection of CD8-expressing thymocytes from 5- to 7-wk-old female PVG.RT1u rats, by rosette depletion with OX8-coated SRBCs (23). The resulting population of cells typically contained 80% single-positive CD4+CD8- thymocytes, 20% CD4-CD8- thymocytes, and <2% contaminating CD8+ cells. CD8-depleted rat thymocytes were further fractionated on the basis of CD25 expression as described above for peripheral CD4+ T cells. Human thymocyte tissue, necessarily removed during cardiac surgery, was obtained from Dr. Katja Simon, Institute of Molecular Medicine (Oxford, U.K.). CD8+ cells were depleted from human thymocytes using OKT8-coated SRBCs.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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In these experiments
CD4+CD45RC- T cells, which
were shown previously to prevent diabetes in TxX
PVG.RT1u rats, were further subdivided on the
basis of CD25 expression. The proportion of CD4+
cells coexpressing CD25 in young adult rats varies slightly between
peripheral tissues, with consistently lower frequencies found in TDL
(Fig. 1
A). Cells expressing
CD25 were predominantly CD45RClow/int, in
contrast with CD25- cells, which were 
70%
CD45RChigh (Fig. 1B). In initial
experiments CD4+CD45RC-
cells, enriched from the spleen and lymph nodes of normal
PVG.RT1u rats and fractionated according to
expression of CD25 (Fig. 2A),
were tested for their ability to protect TxX rats from diabetes.
Depletion of CD25+ cells from the previously
defined CD4+CD45RC-
regulatory T cell population resulted in a loss of the ability of the
remaining cells to protect TxX recipients from diabetes (Fig. 2B). Conversely, positive enrichment of
CD25+ cells from
CD4+CD45RC- cells resulted
in a population of cells able to protect against diabetes at a
reduced cell dose. Thus diabetes-preventing cells were present in the
CD25+ subset of
CD4+CD45RC- T cells, but
the CD25- fraction did not protect. However,
subsequent experiments revealed that this conclusion required important
qualification (below).
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The observation that
CD4+CD45RC-CD25-
T cells from spleen and lymph nodes did not prevent IDDM in prediabetic
recipients (Fig. 2
B) contrasted with previous findings in
this laboratory, in which cells with this phenotype, when isolated from
TDL, did prevent IDDM (2). To reconfirm the previous
result, we repeated the in vivo functional experiments using TDL as a
source of donor T cells and fractionation of cells according to CD25
expression exactly as described for spleen and lymph node cells. In
concordance with the published data, but at variance with the results
obtained using donor cells from spleen and lymph node,
CD4+CD45RC- cells from TDL
protected TxX rats from diabetes even after depletion of
CD25+ cells, indicating that there are regulatory
cells in TDL that are CD25- (Fig. 3). However, CD4+ T
cells enriched for CD25 expression also prevented the development of
diabetes (Fig. 3) at a cell dose lower than that needed for protection
by unfractionated
CD4+CD45RC- cells
(3). It is notable, in the light of these results, that
CD25 is expressed on fewer CD4+ T cells from TDL
compared with spleen and lymph nodes (Fig. 1A).
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It was shown previously in this laboratory that mature CD4+CD8- thymocytes are a potent source of regulatory cells capable of transferring protection against diabetes to TxX rats (3, 24); however, it had not been determined whether the regulatory cells were a phenotypically distinct subset in the thymus or were derived from uncommitted precursors that had been educated in the periphery to become regulatory. Because CD25 expression had been found to be a feature of many of the regulatory cells in the periphery, especially in spleen and lymph nodes, experiments were conducted to determine whether expression of CD25 on CD4+ thymocytes could similarly be used as a marker to distinguish thymocytes capable of preventing autoimmune disease from those mediating other functions.
CD25 expression was examined on thymocytes from 6-wk-old rats and was
found on 6% of
CD4+CD8- thymocytes
(±1.5; n = 4) and 8% of recent thymic emigrants.
Fig. 4 shows this result for thymocytes
together with comparable data on human thymus, in which the CD25
expression profile is very similar (9 ± 1.7%; n
= 3). In the standard adoptive transfer assay, only thymocytes
expressing CD25 were able to protect against the development of
diabetes in TxX rats (Fig. 5). In
contrast, the transfer of CD25-depleted CD8-
thymocytes actually led to acceleration of disease onset
(p < 0.02, by Mann-Whitney two-tailed test),
in confirmation of our earlier determination that some mature
CD4+ thymocytes were diabetogenic
(3). The CD25+ cells responsible for
protection were CD4+CD8-,
because although a minority of
CD4-CD8- cells were also
present in the CD25+ protective inoculum, <1%
of these coexpressed the TCR, and depletion of
CD4+ cells from the
CD8-CD25+ thymocytes
resulted in a population of cells that no longer protected against
diabetes (data not shown). Thus, the
CD4+CD8- thymocytes
capable of preventing autoimmune disease were already phenotypically
and functionally distinct before leaving the thymus. The significance
of this result with regard to the lineage relationship between
CD25+ and CD25- peripheral
regulatory cells will be discussed below.
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The presence of autoreactive cells in the peripheral T cell repertoire of rats, which is revealed by the TxX protocol, raised the question of whether these cells played any useful part in protective immune responses to pathogens or whether their presence simply reflected inefficient clonal deletion in the thymus. In an attempt to examine this question experiments were conducted to determine whether autoreactive T cells could be found in the memory T cell pool. A positive result would be presumptive evidence that they played a useful role.
The CD45RC- subset of CD4+
T cells in rats contains both memory cells and RTE, and early
experiments had provided an indication that the
CD25- subset of these cells led to an
acceleration of diabetes onset. Because RTE would be expected, like
their intrathymic precursors, to contain autoreactive T cells,
CD4+CD45RC-CD25-
T cells were isolated from rats that had been thymectomized 4 wk
previously. As RTE mature to become CD45RC+
within 3–7 days of leaving the thymus (25), the
CD45RC- subset of CD4+ T
cells from donors thymectomized 4 wk previously contains only memory T
cells. It was anticipated that if the memory T cell pool contained
autoreactive T cells, the injection of
CD4+CD45RC-CD25-
T cells from the spleen and lymph nodes of thymectomized donors into
prediabetic recipients would accelerate the onset of diabetes, as
CD4+CD25- thymocytes had
been found to do. Contrary to expectation, the transfer of these
CD25- memory cells from thymectomized rats
prevented diabetes (Fig. 6). This
protection could be attributed to the elimination of RTE from the
CD25-CD45RC- subset of
thymectomized donors, because the same subset purified from the spleen
and lymph nodes of sham-thymectomized control donors was not
protective. In a separate experiment to support these data,
CD45RC-CD25- cells from
normal donors were fractionated into memory cells and RTE by sorting
cells according to expression of Thy1, which in rats is expressed on
RTE and is lost as the cells mature (25).
CD25-Thy1-CD45RC-
(memory) cells (107) from normal donors prevented
diabetes (one in four rats developed diabetes compared with all seven
recipients given no cells; p < 0.01, by one-tailed
log-rank test). The regulatory
CD45RC-CD25- cells
from thymectomized donors were CD4+, because
protection from diabetes was lost upon removal of
CD4+ cells from this subset (data not shown).
Taking these data together, it follows that in peripheral lymphoid
organs the expression of CD25 on CD4+ memory
cells does not identify all cells with regulatory activity. These data
also provide evidence that diabetogenic cells can be found within the
CD4+CD25- RTE
population.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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) from
syngeneic donors can prevent the development of diabetes in TxX
PVG.RT1u recipients. This is true for
CD4+ T cells isolated from both the thymus and
the peripheral lymphoid tissue of rats and is compatible with an
increasing body of data on the phenotype of T cells that prevent
autoimmunity in other disease models in mice (5, 6, 26, 27). Although no functional data for the human thymus are yet
available, the very similar frequency of CD25+
cells in the CD4+CD8-
thymocyte subset of human and rat (Fig. 4) as well as mouse
(27) suggests that the control of autoimmunity in the
three species depends on identical mechanisms.
In the thymus there was no evidence of any protective cells among the
CD25-CD4+ subset. On the
contrary, transfer of this population led to disease acceleration in
prediabetic recipients, supporting the earlier inference that
diabetogenic cells are present in the CD4+
thymocyte subset (3). With peripheral
CD4+ cells the situation is more complex. In
confirmation of earlier experiments (2),
CD25-CD45RC-CD4+
donor cells from TDL could protect TxX recipients from diabetes (Fig. 3). However, as the present experiments show, the transfer of similar
cells from lymph node and spleen did not protect, even at a high cell
dose (Fig. 2B). This latter result is in agreement with
published data in the mouse (5), but appeared paradoxical,
in that TDL is composed of cells that migrate into the lymph from lymph
nodes. The presence of protective CD25- T cells
in lymph node and spleen was revealed by the removal of RTE from the
transferred CD25-CD45RC-
subpopulation either by prior thymectomy of donor animals or by the
removal of Thy1+ cells from the donor inoculum
(Fig. 6). These data indicated that TDL differed from lymph node and
spleen only in the relative ratios of CD25-
regulatory and diabetogenic cells. The reason for this difference is
not known, but it may reflect different recirculation kinetics for
autoreactive T cells and regulatory ones. Alternatively, as discussed
below, the level of expression of CD25 on regulatory T cells may be
down-regulated as the cells migrate from lymph nodes into lymph.
The requirement to remove RTE to demonstrate regulatory T cell activity among CD4+CD45RC-CD25- lymph node and spleen cells (which contain a mixture of RTE and memory T cells) indicates that the balance between autoimmunity and regulation is different in these two T cell populations. This conclusion raises the question of the origin of the CD25- regulatory cells in the memory T cell pool. It follows that any difference in potency among mature peripheral cells with regard to the prevention of autoimmunity can be properly evaluated only when both CD25+ and CD25- regulatory T cells are obtained from peripheral CD4+ T cells depleted of RTE. Nonetheless, the data support the conclusion that the thymus does not export CD25- cells precommitted to a regulatory role and that these cells either acquire their regulatory function in the periphery or derive from CD25+ precursors. If the latter interpretation is the correct one, then CD25 expression is not a stable marker for regulatory T cells in the periphery. While our data do not rule out this conclusion, there are a number of examples in other studies in which regulatory T cells were generated in the periphery by a process of recruitment or infectious tolerance (28). In the mouse, peripheral T cells that prevent skin allograft rejection can be induced by the in vivo coculture of their precursors with established CD4+ regulatory cells (28, 29). While it remains to be determined whether CD25- T cells that prevent diabetes in TxX rats, are recruited from uncommitted precursors, it is probable that the recruitment mechanism, demonstrated in skin allograft tolerance, is an illustration of a process that normally plays a physiological role in the maintenance of self-tolerance.
These allograft tolerance experiments suggest that regulatory T cells generated by infectious tolerance have specificity for the target alloantigens. In this context we have shown that the regulatory CD4+ T cells that prevent autoimmune thyroiditis, while present in the thymus of athyroid rats, are absent in the periphery (4). This result strongly suggests that the readily demonstrable regulatory T cells that prevent thyroiditis in these experiments are specific for thyroid autoantigens. Preliminary data indicate that, as expected, this population is CD25+ (L. Stephens, unpublished observations). No data are yet available regarding the Ag specificity of the CD25- regulatory cells.
Our experiments gave no evidence for the presence of autoreactive T cells among CD4+CD45RC- memory cells. Previous studies from this laboratory have revealed that naive peripheral CD4+CD45RC+ T cells can cause a range of autoimmune diseases (30), and the current experiments demonstrate similarly autoreactive cells among CD4+ thymocytes and RTE. These data together with earlier results on diabetes in TxX rats (2) indicate that the autoimmune diseases that develop in these animals represent at least in part the activation of naive cells. The presence of regulatory T cells in the CD25- memory pool of CD4+ cells prevented determination of the coexistence of any autoreactive T cells in this subset. However, if the CD25- regulatory subset is recruited from uncommitted precursors, as the CD4+ cells that prevent skin allograft rejection in the mouse appear to be (29), then the fate of at least some of the naive autoreactive T cells in normal animals may be to become, after activation, T cells that prevent disease rather than induce it. Currently, the developmental lineage of CD25- regulatory T cells is being studied.
In summary, these studies show that CD25 is a useful marker for regulatory T cells present in the thymus, which are likely to be the precursors of at least some of the CD25+ peripheral regulatory cells. However, our results also demonstrate that CD25 expression in the periphery is not a characteristic of all cells that can control organ-specific autoimmunity. It remains to be determined whether CD25- regulatory cells are induced in the periphery rather than being precommitted to a regulatory role in the thymus. There are possible therapeutic implications in the answer to this question.
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Acknowledgments |
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Footnotes |
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2 Address correspondence and reprint requests to Dr. Leigh Stephens, Sir William Dunn School of Pathology, University of Oxford, Oxford, OX1 3RE U.K.
3 Abbreviations used in this paper: IDDM, insulin-dependent diabetes mellitus; TDL, thoracic duct lymph; TxX, thymectomized and irradiated rats; RTE, recent thymic emigrants; DAM, donkey anti-mouse IgG.
Received for publication April 17, 2000. Accepted for publication July 5, 2000.
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References |
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-chains (CD25): breakdown of a single mechanism of self-tolerance causes various autoimmune diseases. J. Immunol. 155:1151.[Abstract]
chain, resistance to clonal deletion and IL-2 dependency. Int. Immunol. 10:371.This article has been cited by other articles:
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  J. Ji and M. W. Cloyd HIV-1 binding to CD4 on CD4+CD25+ regulatory T cells enhances their suppressive function and induces them to home to, and accumulate in, peripheral and mucosal lymphoid tissues: an additional mechanism of immunosuppression Int. Immunol., March 1, 2009; 21(3): 283 - 294. [Abstract] [Full Text] [PDF]
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 Y. Han, Q. Guo, M. Zhang, Z. Chen, and X. Cao CD69+CD4+CD25- T Cells, a New Subset of Regulatory T Cells, Suppress T Cell Proliferation through Membrane-Bound TGF-{beta}1 J. Immunol., January 1, 2009; 182(1): 111 - 120. [Abstract] [Full Text] [PDF]
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 |
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 N. H. E. Mabarrack, N. L. Turner, and G. Mayrhofer Recent thymic origin, differentiation, and turnover of regulatory T cells J. Leukoc. Biol., November 1, 2008; 84(5): 1287 - 1297. [Abstract] [Full Text] [PDF]
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D. Baatar, P. Olkhanud, K. Sumitomo, D. Taub, R. Gress, and A. Biragyn Human Peripheral Blood T Regulatory Cells (Tregs), Functionally Primed CCR4+ Tregs and Unprimed CCR4- Tregs, Regulate Effector T Cells Using FasL J. Immunol., April 15, 2007; 178(8): 4891 - 4900. [Abstract] [Full Text] [PDF]
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K. N. Couper, D. G. Blount, J. B. de Souza, I. Suffia, Y. Belkaid, and E. M. Riley Incomplete Depletion and Rapid Regeneration of Foxp3+ Regulatory T Cells Following Anti-CD25 Treatment in Malaria-Infected Mice J. Immunol., April 1, 2007; 178(7): 4136 - 4146. [Abstract] [Full Text] [PDF]
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 |
|
 E. Kreijveld, H. J. P. M. Koenen, L. B. Hilbrands, H. J. P. van Hooff, and I. Joosten The immunosuppressive drug FK778 induces regulatory activity in stimulated human CD4+CD25- T cells Blood, January 1, 2007; 109(1): 244 - 252. [Abstract] [Full Text] [PDF]
|
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|
|
|
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S. Sharma, A. L. Dominguez, and J. Lustgarten High Accumulation of T Regulatory Cells Prevents the Activation of Immune Responses in Aged Animals J. Immunol., December 15, 2006; 177(12): 8348 - 8355. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-L. Hillebrands, B. Whalen, J. T. J. Visser, J. Koning, K. D. Bishop, J. Leif, J. Rozing, J. P. Mordes, D. L. Greiner, and A. A. Rossini A Regulatory CD4+ T Cell Subset in the BB Rat Model of Autoimmune Diabetes Expresses Neither CD25 Nor Foxp3 J. Immunol., December 1, 2006; 177(11): 7820 - 7832. [Abstract] [Full Text] [PDF]
|
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|
 |
|
 C. A. Lawson, A. K. Brown, V. Bejarano, S. H. Douglas, C. H. Burgoyne, A. S. Greenstein, A. W. Boylston, P. Emery, F. Ponchel, and J. D. Isaacs Early rheumatoid arthritis is associated with a deficit in the CD4+CD25high regulatory T cell population in peripheral blood Rheumatology, October 1, 2006; 45(10): 1210 - 1217. [Abstract] [Full Text] [PDF]
|
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|
 |
|
 A. Vojdani and J. Erde Regulatory T Cells, a Potent Immunoregulatory Target for CAM Researchers: Modulating Tumor Immunity, Autoimmunity and Alloreactive Immunity (III) Evid. Based Complement. Altern. Med., September 1, 2006; 3(3): 309 - 316. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
K. J. Scalapino, Q. Tang, J. A. Bluestone, M. L. Bonyhadi, and D. I. Daikh Suppression of Disease in New Zealand Black/New Zealand White Lupus-Prone Mice by Adoptive Transfer of Ex Vivo Expanded Regulatory T Cells J. Immunol., August 1, 2006; 177(3): 1451 - 1459. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H. W. Lim, H. E. Broxmeyer, and C. H. Kim Regulation of Trafficking Receptor Expression in Human Forkhead Box P3+ Regulatory T Cells J. Immunol., July 15, 2006; 177(2): 840 - 851. [Abstract] [Full Text] [PDF]
|
|
|
|
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|
M. Ono, J. Shimizu, Y. Miyachi, and S. Sakaguchi Control of Autoimmune Myocarditis and Multiorgan Inflammation by Glucocorticoid-Induced TNF Receptor Family-Related Proteinhigh, Foxp3-Expressing CD25+ and CD25- Regulatory T Cells. J. Immunol., April 15, 2006; 176(8): 4748 - 4756. [Abstract] [Full Text] [PDF]
|
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|
|
 |
|
 U. C. Rogner, F. Lepault, M.-C. Gagnerault, D. Vallois, J. Morin, P. Avner, and C. Boitard The Diabetes Type 1 Locus Idd6 Modulates Activity of CD4+CD25+ Regulatory T-Cells Diabetes, January 1, 2006; 55(1): 186 - 192. [Abstract] [Full Text] [PDF]
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|
|
A. V. Maker, P. Attia, and S. A. Rosenberg Analysis of the Cellular Mechanism of Antitumor Responses and Autoimmunity in Patients Treated with CTLA-4 Blockade J. Immunol., December 1, 2005; 175(11): 7746 - 7754. [Abstract] [Full Text] [PDF]
|
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|
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|
 L. A. Stephens, D. Gray, and S. M. Anderton CD4+CD25+ regulatory T cells limit the risk of autoimmune disease arising from T cell receptor crossreactivity PNAS, November 29, 2005; 102(48): 17418 - 17423. [Abstract] [Full Text] [PDF]
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 U G Strauch, F Obermeier, N Grunwald, S Gurster, N Dunger, M Schultz, D P Griese, M Mahler, J Scholmerich, and H C Rath Influence of intestinal bacteria on induction of regulatory T cells: lessons from a transfer model of colitis Gut, November 1, 2005; 54(11): 1546 - 1552. [Abstract] [Full Text] [PDF]
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 V. Gillan and E. Devaney Regulatory T Cells Modulate Th2 Responses Induced by Brugia pahangi Third-Stage Larvae Infect. Immun., July 1, 2005; 73(7): 4034 - 4042. [Abstract] [Full Text] [PDF]
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H. J. P. M. Koenen, E. Fasse, and I. Joosten CD27/CFSE-Based Ex Vivo Selection of Highly Suppressive Alloantigen-Specific Human Regulatory T Cells J. Immunol., June 15, 2005; 174(12): 7573 - 7583. [Abstract] [Full Text] [PDF]
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S. You, M. Belghith, S. Cobbold, M.-A. Alyanakian, C. Gouarin, S. Barriot, C. Garcia, H. Waldmann, J.-F. Bach, and L. Chatenoud Autoimmune Diabetes Onset Results From Qualitative Rather Than Quantitative Age-Dependent Changes in Pathogenic T-Cells Diabetes, May 1, 2005; 54(5): 1415 - 1422. [Abstract] [Full Text] [PDF]
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Y. Y. Wan and R. A. Flavell Identifying Foxp3-expressing suppressor T cells with a bicistronic reporter PNAS, April 5, 2005; 102(14): 5126 - 5131. [Abstract] [Full Text] [PDF]
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 J. C. Marie, J. J. Letterio, M. Gavin, and A. Y. Rudensky TGF-{beta}1 maintains suppressor function and Foxp3 expression in CD4+CD25+ regulatory T cells J. Exp. Med., April 4, 2005; 201(7): 1061 - 1067. [Abstract] [Full Text] [PDF]
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D. Lundsgaard, T. L. Holm, L. Hornum, and H. Markholst In Vivo Control of Diabetogenic T-Cells by Regulatory CD4+CD25+ T-Cells Expressing Foxp3 Diabetes, April 1, 2005; 54(4): 1040 - 1047. [Abstract] [Full Text] [PDF]
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P. Poussier, T. Ning, T. Murphy, D. Dabrowski, and S. Ramanathan Impaired Post-Thymic Development of Regulatory CD4+25+ T Cells Contributes to Diabetes Pathogenesis in BB Rats J. Immunol., April 1, 2005; 174(7): 4081 - 4089. [Abstract] [Full Text] [PDF]
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J. Shimizu, R. Iida, Y. Sato, E. Moriizumi, A. Nishikawa, and Y. Ishida Cross-Linking of CD45 on Suppressive/Regulatory T Cells Leads to the Abrogation of Their Suppressive Activity In Vitro J. Immunol., April 1, 2005; 174(7): 4090 - 4097. [Abstract] [Full Text] [PDF]
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M. P. Eggena, B. Barugahare, N. Jones, M. Okello, S. Mutalya, C. Kityo, P. Mugyenyi, and H. Cao Depletion of Regulatory T Cells in HIV Infection Is Associated with Immune Activation J. Immunol., April 1, 2005; 174(7): 4407 - 4414. [Abstract] [Full Text] [PDF]
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A. Bushell, E. Jones, A. Gallimore, and K. Wood The Generation of CD25+CD4+ Regulatory T Cells That Prevent Allograft Rejection Does Not Compromise Immunity to a Viral Pathogen J. Immunol., March 15, 2005; 174(6): 3290 - 3297. [Abstract] [Full Text] [PDF]
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P. E. Rao, A. L. Petrone, and P. D. Ponath Differentiation and Expansion of T Cells with Regulatory Function from Human Peripheral Lymphocytes by Stimulation in the Presence of TGF-{beta} J. Immunol., February 1, 2005; 174(3): 1446 - 1455. [Abstract] [Full Text] [PDF]
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M. A. Curotto de Lafaille, A. C. Lino, N. Kutchukhidze, and J. J. Lafaille CD25- T Cells Generate CD25+Foxp3+ Regulatory T Cells by Peripheral Expansion J. Immunol., December 15, 2004; 173(12): 7259 - 7268. [Abstract] [Full Text] [PDF]
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E. Xystrakis, A. S. Dejean, I. Bernard, P. Druet, R. Liblau, D. Gonzalez-Dunia, and A. Saoudi Identification of a novel natural regulatory CD8 T-cell subset and analysis of its mechanism of regulation Blood, November 15, 2004; 104(10): 3294 - 3301. [Abstract] [Full Text] [PDF]
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H. C. Dujardin, O. Burlen-Defranoux, L. Boucontet, P. Vieira, A. Cumano, and A. Bandeira Regulatory potential and control of Foxp3 expression in newborn CD4+ T cells PNAS, October 5, 2004; 101(40): 14473 - 14478. [Abstract] [Full Text] [PDF]
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S. Makita, T. Kanai, S. Oshima, K. Uraushihara, T. Totsuka, T. Sawada, T. Nakamura, K. Koganei, T. Fukushima, and M. Watanabe CD4+CD25bright T Cells in Human Intestinal Lamina Propria as Regulatory Cells J. Immunol., September 1, 2004; 173(5): 3119 - 3130. [Abstract] [Full Text] [PDF]
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E. Nishimura, T. Sakihama, R. Setoguchi, K. Tanaka, and S. Sakaguchi Induction of antigen-specific immunologic tolerance by in vivo and in vitro antigen-specific expansion of naturally arising Foxp3+CD25+CD4+ regulatory T cells Int. Immunol., August 1, 2004; 16(8): 1189 - 1201. [Abstract] [Full Text] [PDF]
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M. A. Lerman, J. Larkin III, C. Cozzo, M. S. Jordan, and A. J. Caton CD4+ CD25+ Regulatory T Cell Repertoire Formation in Response to Varying Expression of a neo-Self-Antigen J. Immunol., July 1, 2004; 173(1): 236 - 244. [Abstract] [Full Text] [PDF]
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I. Apostolou and H. von Boehmer In Vivo Instruction of Suppressor Commitment in Naive T Cells J. Exp. Med., May 17, 2004; 199(10): 1401 - 1408. [Abstract] [Full Text] [PDF]
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I. M. de Kleer, L. R. Wedderburn, L. S. Taams, A. Patel, H. Varsani, M. Klein, W. de Jager, G. Pugayung, F. Giannoni, G. Rijkers, et al. CD4+CD25bright Regulatory T Cells Actively Regulate Inflammation in the Joints of Patients with the Remitting Form of Juvenile Idiopathic Arthritis J. Immunol., May 15, 2004; 172(10): 6435 - 6443. [Abstract] [Full Text] [PDF]
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T. W. Vahlenkamp, M. B. Tompkins, and W. A. F. Tompkins Feline Immunodeficiency Virus Infection Phenotypically and Functionally Activates Immunosuppressive CD4+CD25+ T Regulatory Cells J. Immunol., April 15, 2004; 172(8): 4752 - 4761. [Abstract] [Full Text] [PDF]
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M. W. Beilharz, L. M. Sammels, A. Paun, K. Shaw, P. van Eeden, M. W. Watson, and M. L. Ashdown Timed Ablation of Regulatory CD4+ T Cells Can Prevent Murine AIDS Progression J. Immunol., April 15, 2004; 172(8): 4917 - 4925. [Abstract] [Full Text] [PDF]
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B. H. Nelson IL-2, Regulatory T Cells, and Tolerance J. Immunol., April 1, 2004; 172(7): 3983 - 3988. [Abstract] [Full Text] [PDF]
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F. Kajiura, S. Sun, T. Nomura, K. Izumi, T. Ueno, Y. Bando, N. Kuroda, H. Han, Y. Li, A. Matsushima, et al. NF-{kappa}B-Inducing Kinase Establishes Self-Tolerance in a Thymic Stroma-Dependent Manner J. Immunol., February 15, 2004; 172(4): 2067 - 2075. [Abstract] [Full Text] [PDF]
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L. A. Stephens, A. N. Barclay, and D. Mason Phenotypic characterization of regulatory CD4+CD25+ T cells in rats Int. Immunol., February 1, 2004; 16(2): 365 - 375. [Abstract] [Full Text] [PDF]
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H. Jonuleit and E. Schmitt The Regulatory T Cell Family: Distinct Subsets and their Interrelations J. Immunol., December 15, 2003; 171(12): 6323 - 6327. [Full Text] [PDF]
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E. S. Yvon, S. Vigouroux, R. F. Rousseau, E. Biagi, P. Amrolia, G. Dotti, H.-J. Wagner, and M. K. Brenner Overexpression of the Notch ligand, Jagged-1, induces alloantigen-specific human regulatory T cells Blood, November 15, 2003; 102(10): 3815 - 3821. [Abstract] [Full Text] [PDF]
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E. Anastasi, A. F. Campese, D. Bellavia, A. Bulotta, A. Balestri, M. Pascucci, S. Checquolo, R. Gradini, U. Lendahl, L. Frati, et al. Expression of Activated Notch3 in Transgenic Mice Enhances Generation of T Regulatory Cells and Protects against Experimental Autoimmune Diabetes J. Immunol., November 1, 2003; 171(9): 4504 - 4511. [Abstract] [Full Text] [PDF]
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W. Janssens, V. Carlier, B. Wu, L. VanderElst, M. G. Jacquemin, and J.-M. R. Saint-Remy CD4+CD25+ T Cells Lyse Antigen-Presenting B Cells by Fas-Fas Ligand Interaction in an Epitope-Specific Manner J. Immunol., November 1, 2003; 171(9): 4604 - 4612. [Abstract] [Full Text] [PDF]
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B. Dubois, L. Chapat, A. Goubier, M. Papiernik, J.-F. Nicolas, and D. Kaiserlian Innate CD4+CD25+ regulatory T cells are required for oral tolerance and inhibition of CD8+ T cells mediating skin inflammation Blood, November 1, 2003; 102(9): 3295 - 3301. [Abstract] [Full Text] [PDF]
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S. Gregori, N. Giarratana, S. Smiroldo, and L. Adorini Dynamics of Pathogenic and Suppressor T Cells in Autoimmune Diabetes Development J. Immunol., October 15, 2003; 171(8): 4040 - 4047. [Abstract] [Full Text] [PDF]
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P. Feunou, L. Poulin, C. Habran, A. Le Moine, M. Goldman, and M. Y. Braun CD4+CD25+ and CD4+CD25- T Cells Act Respectively as Inducer and Effector T Suppressor Cells in Superantigen-Induced Tolerance J. Immunol., October 1, 2003; 171(7): 3475 - 3484. [Abstract] [Full Text] [PDF]
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H. von Boehmer Dynamics of Suppressor T Cells: In Vivo Veritas J. Exp. Med., September 15, 2003; 198(6): 845 - 849. [Full Text] [PDF]
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T. Mizobuchi, K. Yasufuku, Y. Zheng, M. A. Haque, K. M. Heidler, K. Woods, G. N. Smith Jr., O. W. Cummings, T. Fujisawa, J. S. Blum, et al. Differential Expression of Smad7 Transcripts Identifies the CD4+CD45RChigh Regulatory T Cells That Mediate Type V Collagen-Induced Tolerance to Lung Allografts J. Immunol., August 1, 2003; 171(3): 1140 - 1147. [Abstract] [Full Text] [PDF]
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L. Klein, K. Khazaie, and H. von Boehmer In vivo dynamics of antigen-specific regulatory T cells not predicted from behavior in vitro PNAS, July 22, 2003; 100(15): 8886 - 8891. [Abstract] [Full Text] [PDF]
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K. Uraushihara, T. Kanai, K. Ko, T. Totsuka, S. Makita, R. Iiyama, T. Nakamura, and M. Watanabe Regulation of Murine Inflammatory Bowel Disease by CD25+ and CD25- CD4+ Glucocorticoid-Induced TNF Receptor Family-Related Gene+ Regulatory T Cells J. Immunol., July 15, 2003; 171(2): 708 - 716. [Abstract] [Full Text] [PDF]
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C. Asseman, S. Read, and F. Powrie Colitogenic Th1 Cells Are Present in the Antigen-Experienced T Cell Pool in Normal Mice: Control by CD4+ Regulatory T Cells and IL-10 J. Immunol., July 15, 2003; 171(2): 971 - 978. [Abstract] [Full Text] [PDF]
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N. A. Marshall, M. A. Vickers, and R. N. Barker Regulatory T Cells Secreting IL-10 Dominate the Immune Response to EBV Latent Membrane Protein 1 J. Immunol., June 15, 2003; 170(12): 6183 - 6189. [Abstract] [Full Text] [PDF]
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W. W. J. Unger, W. Jansen, D. A. W. Wolvers, A. G. S. van Halteren, G. Kraal, and J. N. Samsom Nasal tolerance induces antigen-specific CD4+CD25- regulatory T cells that can transfer their regulatory capacity to naive CD4+ T cells Int. Immunol., June 1, 2003; 15(6): 731 - 739. [Abstract] [Full Text] [PDF]
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M. Paas-Rozner, M. Sela, and E. Mozes A dual altered peptide ligand down-regulates myasthenogenic T cell responses by up-regulating CD25- and CTLA-4-expressing CD4+ T cells PNAS, May 27, 2003; 100(11): 6676 - 6681. [Abstract] [Full Text] [PDF]
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S. Grundstrom, L. Cederbom, A. Sundstedt, P. Scheipers, and F. Ivars Superantigen-Induced Regulatory T Cells Display Different Suppressive Functions in the Presence or Absence of Natural CD4+CD25+ Regulatory T Cells In Vivo J. Immunol., May 15, 2003; 170(10): 5008 - 5017. [Abstract] [Full Text] [PDF]
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T. Oida, X. Zhang, M. Goto, S. Hachimura, M. Totsuka, S. Kaminogawa, and H. L. Weiner CD4+CD25- T Cells That Express Latency-Associated Peptide on the Surface Suppress CD4+CD45RBhigh-Induced Colitis by a TGF-{beta}-Dependent Mechanism J. Immunol., March 1, 2003; 170(5): 2516 - 2522. [Abstract] [Full Text] [PDF]
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T. Barthlott, G. Kassiotis, and B. Stockinger T Cell Regulation as a Side Effect of Homeostasis and Competition J. Exp. Med., February 17, 2003; 197(4): 451 - 460. [Abstract] [Full Text] [PDF]
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J. Shimizu and E. Moriizumi CD4+CD25- T Cells in Aged Mice Are Hyporesponsive and Exhibit Suppressive Activity J. Immunol., February 15, 2003; 170(4): 1675 - 1682. [Abstract] [Full Text] [PDF]
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 S. Hori, T. Nomura, and S. Sakaguchi Control of Regulatory T Cell Development by the Transcription Factor Foxp3 Science, February 14, 2003; 299(5609): 1057 - 1061. [Abstract] [Full Text] [PDF]
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K. J. Maloy, L. Salaun, R. Cahill, G. Dougan, N. J. Saunders, and F. Powrie CD4+CD25+ TR Cells Suppress Innate Immune Pathology Through Cytokine-dependent Mechanisms J. Exp. Med., January 6, 2003; 197(1): 111 - 119. [Abstract] [Full Text] [PDF]
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S. G. Zheng, J. D. Gray, K. Ohtsuka, S. Yamagiwa, and D. A. Horwitz Generation Ex Vivo of TGF-{beta}-Producing Regulatory T Cells from CD4+CD25- Precursors J. Immunol., October 15, 2002; 169(8): 4183 - 4189. [Abstract] [Full Text] [PDF]
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 M. Schwartz and J. Kipnis Multiple Sclerosis as a By-Product of the Failure to Sustain Protective Autoimmunity: A Paradigm Shift Neuroscientist, October 1, 2002; 8(5): 405 - 413. [Abstract] [PDF]
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J. Lehmann, J. Huehn, M. de la Rosa, F. Maszyna, U. Kretschmer, V. Krenn, M. Brunner, A. Scheffold, and A. Hamann Expression of the integrin alpha Ebeta 7 identifies unique subsets of CD25+ as well as CD25- regulatory T cells PNAS, October 1, 2002; 99(20): 13031 - 13036. [Abstract] [Full Text] [PDF]
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V. Szanya, J. Ermann, C. Taylor, C. Holness, and C. G. Fathman The Subpopulation of CD4+CD25+ Splenocytes That Delays Adoptive Transfer of Diabetes Expresses L-Selectin and High Levels of CCR7 J. Immunol., September 1, 2002; 169(5): 2461 - 2465. [Abstract] [Full Text] [PDF]
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M. C. Kullberg, D. Jankovic, P. L. Gorelick, P. Caspar, J. J. Letterio, A. W. Cheever, and A. Sher Bacteria-triggered CD4+ T Regulatory Cells Suppress Helicobacter hepaticus-induced Colitis J. Exp. Med., August 19, 2002; 196(4): 505 - 515. [Abstract] [Full Text] [PDF]
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P. Hoffmann, J. Ermann, M. Edinger, C. G. Fathman, and S. Strober Donor-type CD4+CD25+ Regulatory T Cells Suppress Lethal Acute Graft-Versus-Host Disease after Allogeneic Bone Marrow Transplantation J. Exp. Med., August 5, 2002; 196(3): 389 - 399. [Abstract] [Full Text] [PDF]
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J. L. Cohen, A. Trenado, D. Vasey, D. Klatzmann, and B. L. Salomon CD4+CD25+ Immunoregulatory T Cells: New Therapeutics for Graft-Versus-Host Disease J. Exp. Med., August 5, 2002; 196(3): 401 - 406. [Abstract] [Full Text] [PDF]
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M. Murakami, A. Sakamoto, J. Bender, J. Kappler, and P. Marrack CD25+CD4+ T cells contribute to the control of memory CD8+ T cells PNAS, June 25, 2002; 99(13): 8832 - 8837. [Abstract] [Full Text] [PDF]
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S. Hori, M. Haury, A. Coutinho, and J. Demengeot Specificity requirements for selection and effector functions of CD25+4+ regulatory T cells in anti-myelin basic protein T cell receptor transgenic mice PNAS, June 11, 2002; 99(12): 8213 - 8218. [Abstract] [Full Text] [PDF]
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L. Graca, S. Thompson, C.-Y. Lin, E. Adams, S. P. Cobbold, and H. Waldmann Both CD4+CD25+ and CD4+CD25- Regulatory Cells Mediate Dominant Transplantation Tolerance J. Immunol., June 1, 2002; 168(11): 5558 - 5565. [Abstract] [Full Text] [PDF]
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E. Jimenez, R. Sacedon, A. Vicente, C. Hernandez-Lopez, A. G. Zapata, and A. Varas Rat Peripheral CD4+CD8+ T Lymphocytes Are Partially Immunocompetent Thymus-Derived Cells That Undergo Post-Thymic Maturation to Become Functionally Mature CD4+ T Lymphocytes J. Immunol., May 15, 2002; 168(10): 5005 - 5013. [Abstract] [Full Text] [PDF]
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E. Chiffoleau, G. Beriou, P. Dutartre, C. Usal, J.-P. Soulillou, and M. C. Cuturi Role for Thymic and Splenic Regulatory CD4+ T Cells Induced by Donor Dendritic Cells in Allograft Tolerance by LF15-0195 Treatment J. Immunol., May 15, 2002; 168(10): 5058 - 5069. [Abstract] [Full Text] [PDF]
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S. Gregori, N. Giarratana, S. Smiroldo, M. Uskokovic, and L. Adorini A 1{alpha},25-Dihydroxyvitamin D3 Analog Enhances Regulatory T-Cells and Arrests Autoimmune Diabetes in NOD Mice Diabetes, May 1, 2002; 51(5): 1367 - 1374. [Abstract] [Full Text] [PDF]
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C. I. Kingsley, M. Karim, A. R. Bushell, and K. J. Wood CD25+CD4+ Regulatory T Cells Prevent Graft Rejection: CTLA-4- and IL-10-Dependent Immunoregulation of Alloresponses J. Immunol., February 1, 2002; 168(3): 1080 - 1086. [Abstract] [Full Text] [PDF]
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J. M. Phillips, N. M. Parish, M. Drage, and A. Cooke Cutting Edge: Interactions Through the IL-10 Receptor Regulate Autoimmune Diabetes J. Immunol., December 1, 2001; 167(11): 6087 - 6091. [Abstract] [Full Text] [PDF]
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M. A. C. de Lafaille, S. Muriglan, M.-J. Sunshine, Y. Lei, N. Kutchukhidze, G. C. Furtado, A. K. Wensky, D. Olivares-Villagomez, and J. J. Lafaille Hyper Immunoglobulin E Response in Mice with Monoclonal Populations of B and T Lymphocytes"" J. Exp. Med., November 5, 2001; 194(9): 1349 - 1360. [Abstract] [Full Text] [PDF]
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X. Zhang, L. Izikson, L. Liu, and H. L. Weiner Activation of CD25+CD4+ Regulatory T Cells by Oral Antigen Administration J. Immunol., October 15, 2001; 167(8): 4245 - 4253. [Abstract] [Full Text] [PDF]
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R. P.M. Sutmuller, L. M. van Duivenvoorde, A. van Elsas, T. N.M. Schumacher, M. E. Wildenberg, J. P. Allison, R. E.M. Toes, R. Offringa, and C. J.M. Melief Synergism of Cytotoxic T Lymphocyte-associated Antigen 4 Blockade and Depletion of CD25+ Regulatory T Cells in Antitumor Therapy Reveals Alternative Pathways for Suppression of Autoreactive Cytotoxic T Lymphocyte Responses J. Exp. Med., September 17, 2001; 194(6): 823 - 832. [Abstract] [Full Text] [PDF]
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C. Baecher-Allan, J. A. Brown, G. J. Freeman, and D. A. Hafler CD4+CD25high Regulatory Cells in Human Peripheral Blood J. Immunol., August 1, 2001; 167(3): 1245 - 1253. [Abstract] [Full Text] [PDF]
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F.-D. Shi, M. Flodstrom, B. Balasa, S. H. Kim, K. Van Gunst, J. L. Strominger, S. B. Wilson, and N. Sarvetnick Germ line deletion of the CD1 locus exacerbates diabetes in the NOD mouse PNAS, June 5, 2001; 98(12): 6777 - 6782. [Abstract] [Full Text] [PDF]
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E. M. Shevach Certified Professionals: CD4+CD25+ Suppressor T Cells J. Exp. Med., June 4, 2001; 193(11): F41 - F46. [Full Text] [PDF]
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O. Annacker, R. Pimenta-Araujo, O. Burlen-Defranoux, T. C. Barbosa, A. Cumano, and A. Bandeira CD25+ CD4+ T Cells Regulate the Expansion of Peripheral CD4 T Cells Through the Production of IL-10 J. Immunol., March 1, 2001; 166(5): 3008 - 3018. [Abstract] [Full Text] [PDF]
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4). No differences were noted
between male and female rats. B, Expression of CD45RC on
CD4+CD25+ cells. Shown is the profile of CD45RC
expression on lymph node cells after gating on
CD4+CD25+ cells (bold line) or
CD4+CD25- cells (normal line). This profile is
also representative of cell surface analysis of cells from spleen and
TDL.
