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Departments of
*
Cell Biology and Histology and
Dermatology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands;
Department of Infectious Disease and Immunology, Okinawa-Asia Research Center of Medical Sciences, Faculty of Medicine, University of the Ryukyus, Okinawa, Japan; and
Department of Parasitology, Medical Center Leiden, Leiden, The Netherlands
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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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-producing Th1 cells and IL-4-producing Th2 cells,
which develop from a common pool of naive precursor T cells. There is
accumulating evidence that microbes drive the development of protective
Th1 or Th2 cells through their effects on APCs (1, 2, 3, 4).
Dendritic cells (DCs)3
are professional APCs that are present as immature sentinel cells that
efficiently sample their environment for foreign Ag at potential sites
of pathogen entry. Upon activation by signals released from the
microorganisms or from infected tissues, sentinel DCs undergo
maturation into potent T cell stimulatory effector DCs and migrate
toward the T cell areas of draining lymphoid organs. There, effector
DCs will activate naive Th cells with pathogen-specific (MHC peptide
complexes, signal 1) and costimulatory (B7 family molecules, signal 2)
(5) molecules. In addition to signals 1 and 2, DCs carry a
third signal, which determines the polarization of naive Th cells into
Th1 or Th2 cells (6). Like signal 2, signal 3 is
heterogeneous and can be mediated by various soluble or membrane-bound
molecules, including IL-12 (7), IL-18 (8),
IFN-
(9), and OX40 ligand (OX40L) (10).
Importantly, in vitro studies suggested that the expression levels of
these Th cell-polarizing molecules by mature effector DCs strongly
depend on the conditions during their initial activation as sentinel
DCs. Tissue-derived factors such as IFN- and
PGE2 present during the activation of human
monocyte-derived sentinel DCs promote the generation of type 1 effector
DCs (DC1s), which produce high amounts of IL-12 upon subsequent
engagement of naive T cells, or the generation of IL-12-deficient DC2s,
which drive the development of Th2 cells (11, 12). These
findings imply that pathogens may promote the development of distinct
DC phenotypes by provoking tissues to release mediators involved in
polarization. In addition to these indirect effects, microorganisms also directly affect sentinel DCs at the time of pathogen encounter, as has been shown previously (1, 2, 3, 4).
In the present study, we investigate the DC-derived molecules involved in Th-cell polarization of different DC1 and DC2 subsets. Soluble egg Ags (SEA) of the helminth Schistosoma mansoni and the toxin of the intestinal bacterium Vibrio cholerae (CT), both associated with Th2 cell responses (13, 14), as well as dsRNA (poly(I:C), a mimic of viral RNA) and the toxin of the intracellular bacterium Bordetella pertussis (PT), both associated with Th1 cell responses (15), all promoted sentinel DCs to develop into functional effector cells with stably polarized DC2 or DC1 phenotypes, respectively. It became clear that, although the effector DC1 or DC2 populations induced similar Th1 and Th2 cell subsets, there is a heterogeneity within DC1 and DC2 subsets with respect to the expression and use of Th-polarizing molecules.
The present study indicates that a protective immune response is mounted via the development of polarized DC1 and DC2 subsets with diverse expression of signal 3 induced by factors derived from the invading pathogen.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Monocytes were isolated from PBMCs using density centrifugation.
Immature DCs were generated by culturing monocytes for 6 days in IMDM
(Life Technologies, Paisley, U.K.) containing gentamicin (86 µg/L;
Duchefa, Haarlem, The Netherlands) and 1% FCS (HyClone, Logan, UT),
supplemented with GM-CSF (500 U/ml; Schering-Plough, Uden, The
Netherlands) and IL-4 (250 U/ml; PBH, Hanover, Germany). At day 6,
maturation was induced by culturing the cells for 2 days with the
following factors alone or with a combination as indicated in the text:
IL-1
(10 ng/ml; PBH), TNF- (50 ng/ml; PBH), poly(I:C) (20
µg/ml, Sigma-Aldrich, St. Louis, MO), Schistosoma
mansoni egg Ags (30 µg/ml; prepared as described
previously (16)), CT (1 µg/ml; Sigma-Aldrich), PT (1
µg/ml; Sigma-Aldrich), IFN- (1000 U/ml; gift from Dr. P. H.
van der Meide, Utrecht University, Utrecht, The Netherlands), or
PGE2 (10-6 M;
Sigma-Aldrich). All subsequent tests were performed after harvesting
and extensive washing of the cells to remove all factors.
Expression of cell surface molecules
At day 8, the obtained effector DCs were analyzed for the expression of cell surface molecules by FACS. Mouse anti-human mAbs were used against the following molecules: CD1a (OKT6; Ortho Diagnostic Systems, Beerse, Belgium), CD83 (HB15a, IgG2b; Immunotech, Marseille, France), CD86 (1G10, IgG2a; Innogenetics, Ghent, Belgium), HLA-DR (L234, IgG2a; BD Biosciences, San Jose, CA), and OX40L (5A8) (17). All mAbs were followed by FITC-conjugated goat F(ab')2 anti-mouse IgG and IgM (Jackson ImmunoResearch Laboratories, West Grove, PA). Samples were analyzed on a FACScan (BD Biosciences).
Determination of naive CD4+CD45RA+CD45RO- Th cell polarization by effector DCs
Highly purified
CD4+CD45RA+CD45RO-
naive Th cells (>98% as assessed by flow cytometry) were purified
from PBMCs or PBLs using a human
CD4+/CD45RO- column kit
(R&D Systems, Minneapolis, MN). Naive CD4+ Th
cells (2 x 104 cells/200 µl of IMDM with
10% FCS) were cocultured with 5 x 103
effector DCs coated with Staphylococcus enterotoxin B (SEB;
Sigma-Aldrich; final concentration, 100 pg/ml) in 96-well flat-bottom
culture plates (Costar, Cambridge, MA). As indicated in certain
figures, the following neutralizing or blocking Abs were used:
anti-IL-12 (10 µg/ml; kind gift from Dr. P. H. van der
Meide), anti-IL-18 (10 µg/ml; MBL, Nagoya, Japan),
anti-IFN- (10 µg/ml; PBL, New Brunswick, NJ), and
anti-type I IFNR (10 µg/ml; Research Diagnostics, Flanders, NJ).
At day 5, human rIL-2 (10 U/ml, Cetus, Emeryville, CA) was added, and
the cultures were expanded for the next 9 days. On day 14, the
quiescent Th cells were restimulated with PMA (10 ng/ml; Sigma-Aldrich)
and ionomycin (1 µg/ml; Sigma-Aldrich) for 6 h, and during the
last 5 h, Brefeldin A (10 µg/ml; Sigma-Aldrich) was present to
detect the intracellular production of IL-4 and IFN- (BD
Biosciences). For the direct stimulation of naive Th cells in the
presence of supernatants of activated DCs, plate-bound anti-CD3
(16A9; Central Laboratory for Blood Transfusions, Amsterdam, The
Netherlands) and anti-CD28 (5E8, CLB) were used at a concentration
of 1 µg/ml.
Induction of cytokine production by DCs
CD1a+ DCs (4 x
104 cells/well) were stimulated with human CD40
ligand (CD40L)-expressing mouse fibroblasts (J558 cells; 4 x
104 cells/well; kind gift from Dr. P. Lane,
University of Birmingham, Birmingham, U.K.) in the presence or absence
of human rIFN- (1000 U/ml) in 96-well flat-bottom culture plates
(Costar) in IMDM containing 10% FCS in a final volume of 200 µl.
Supernatants were harvested after 24 h and stored at -20°C
until the levels of cytokines were measured by ELISA.
Cytokine measurements
Measurements of IL-12p70, TNF-, and IL-6 levels in the
culture supernatants were performed by specific solid-phase sandwich
ELISA as described previously (11). The limits of
detection of these ELISAs are as follows: IL-12p70, 3 pg/ml; TNF-,
10 pg/ml; IL-6, 20 pg/ml.
Statistical analysis
Data were analyzed for statistical significance (GraphPad, InStat, version 2.02) using ANOVA followed by Dunnett’s multiple comparisons test. A p value <0.05 was taken as the level of significance.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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To study the direct effects of different microbial compounds on
the maturation of sentinel DCs into effector DCs, uncommitted
monocyte-derived DCs were cultured in the presence of SEA, CT, PT, or
poly(I:C). As a control, DCs were cultured by the combination of
IL-1 and TNF- (maturation-inducing factors (MF)). In agreement
with previous reports, MF (18), CT (4), and
poly(I:C) (1) induced final DC maturation within 48
h, as was evident from the loss of expression of the mannose receptor,
the inability to phagocytose, the induction of CD83 expression, and the
up-regulation of the CD80, CD86, and HLA-DR expression, of which the
expression levels were comparable within the different DC subsets (Fig. 1
A; data not shown for HLA-DR
and CD80). SEA and PT induced DC maturation as well (Fig. 1A), although the degree of maturation in the case of PT
varied among different donors. Because the state of maturation of DCs
may influence the capacity to drive Th1 or Th2 responses, due to
differences in the expression of certain cytokines or membrane-bound
molecules, MF were added to the stimulations (CT, PT, and the controls
PGE2 and IFN-) that do not induce full
maturation by themselves.
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expression (Fig. 1
B). As expected, DCs matured by MF induced
the development of a mixture of IFN--producing Th1 and
IL-4-producing Th2 effector cells. In contrast, DCs matured by SEA or
CT became type 2 DCs (DC2s) with the intrinsic ability to bias for the
development of Th2 cells, comparable to the known Th2-polarizing effect
of PGE2. In contrast, priming of DCs with PT or
poly(I:C) resulted in type 1 DCs (DC1s) that biased for the development
of Th1 cells. The latter effect was comparable to the induction of Th1
cells by DCs matured with the combination of MF and IFN-. Cytokine production by DC subsets
Because the level of IL-12 production by myeloid DCs during
activation of naive Th cells is a major factor driving the development
of Th1 cells, we first studied whether DC1 and DC2 types are associated
with high or low IL-12 production. Bioactive IL-12p70 production by the
effector DC was measured upon ligation of CD40 by CD40L-transfected
cells, thereby mimicking the engagement by T cells (Fig. 2A). Compared with the
MF-primed control DCs, the SEA- or CT-primed DC2s showed a strongly
reduced IL-12p70 production, in accordance with their Th2-driving
capacity. As expected from their Th1-polarizing effect, PT primed for
DC1 with enhanced IL-12p70 production, similar to MF plus
IFN--primed DC1s. Surprisingly, unlike the MF + PT- and MF +
IFN--primed DC1s, poly(I:C)-primed DC1s did not show enhanced
IL-12p70 production, despite their potent Th1-promoting capacity,
suggesting the existence of alternative Th1-driving mechanisms. Priming
of DCs with SEA or poly(I:C) in the additional presence of MF did not
alter the capacity to produce IL-12p70 upon CD40 ligation of the
effector cells (data not shown).
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followed the
pattern of IL-12 production, with the exception that the TNF-
production was consistently not enhanced in PT-primed DCs (Fig. 2B). IL-6 production is differentially regulated (Fig. 2C), being consistently low in SEA-primed DCs and high in
poly(I:C)-primed DCs but unaffected in the other effector DCs. The
production of IFN- by all effector DC subsets was below or near the
detection limit of the ELISA (data not shown). These findings indicate
that the various subsets of DC1 and DC2 have unique cytokine profiles.
Among others, SEA-primed DCs are unable to produce high levels of any
of the cytokines tested (e.g., IL-12, TNF-, and IL-6). The variable
profiles may imply that the microbial compounds activate different
signaling pathways in the sentinel DCs. Role of IL-12 in the induction of Th1 cells
To analyze the contribution of DC-derived IL-12 to the development
of Th1 cells, we tested the effect of neutralizing anti-IL-12 Ab in
cocultures of naive Th cells and the distinct effector DC subsets (Fig. 3, A and B). In the
case of most DC subsets, neutralization of IL-12 increased the
development of IL-4-producing Th cells and dramatically decreased the
development of IFN--producing Th cells. However, in the case of
poly(I:C)-primed DCs, the percentage of IFN--producing cells could
not be reduced below 20–40%. This is in line with the finding that
poly(I:C) primes for efficient effector DC1s despite moderate IL-12
production and suggests that poly(I:C)-primed DCs express Th1-driving
factors other than IL-12p70. Neutralizing Abs to IL-18, IFN-, or
type I IFNR did not substantially block Th1 development induced by the
poly(I:C)-primed DCs (Fig. 3B), suggesting the involvement
of yet another factor.
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In an attempt to further define the Th1- and Th2-driving molecules
expressed by the various effector DC types, we tested to what extent
soluble factors were critical. Supernatants of CD40L-activated DCs
(after 24 h) were added to cultures of naive T cells stimulated
with anti-CD3 and anti-CD28 Abs. After 10–14 days, the
effector Th cells were restimulated, and the IL-4 and IFN-
expression was determined. Supernatants of MF + IFN--primed DCs
strongly promoted the development of Th1 cells, which could be almost
completely blocked by IL-12 Ab (Fig. 4).
Likewise, the supernatants of the poly(I:C)-primed DCs supported the
development of Th1 cells. However, this effect could only be partially
blocked by anti-IL-12 Ab, indicating that the Th1-promoting
activity of these DCs is mediated by an unknown soluble factor.
Supernatants of CD40L-activated DC2s primed with the combination of MF
and PGE2 or with CT exhibited a strong
Th2-driving capacity. This activity could not be blocked by
neutralizing Abs to IL-4, IL-13, or monocyte chemoattractant
protein-1 or by preventing the production of eicosanoids (e.g.,
PGE2) by these DC2s (data not shown). In
contrast, supernatants of CD40L-stimulated SEA-primed DCs failed to
support Th2 development, indicating that these cells exert the Th2 bias
via a membrane-bound factor.
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In the search for the identity of the Th2-driving, membrane-bound
factor on the SEA-primed DC, we focused on OX40L, a factor known to be
expressed by part of the peripheral blood DC and involved in Th2 cell
development (10). Interestingly, OX40L was detectable only
in DC2s and not on any of the DC1 types (Fig. 5A). Even after CD40 ligation,
which has been described to strongly up-regulate OX40L expression, only
a small minority of the cells expressed OX40L, whereas all DC2 cells
showed enhanced OX40L expression (Fig. 5A).
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-producing Th cells
(Fig. 5B). DC1 and DC2 have stable IL-12 secretion profiles
To study the stability of the functional phenotype of the various
types of effector DCs, we tested whether IL-12 production was altered
after stimulation by microbial compounds or cytokines that polarize
immature DCs in the opposite direction. Because the pathogenic factors,
except for poly(I:C), modulate the cytokine production of immature DCs
but do not induce cytokine by themselves (data not shown), the effector
DCs were activated with CD40L in the absence or presence of SEA, CT,
PGE2, or IFN- or with poly(I:C) alone. As
shown in Fig. 6, the IL-12 levels of the
various DC1s and DC2s are largely preserved in any condition of
stimulation. In general, in the presence of compounds that prime for
high IL-12, the IL-12 production was enhanced in DC1s but hardly or not
at all in DC2s. In the presence of down-regulators of IL-12 production,
the IL-12 levels were unchanged or only marginally decreased.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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DC1 primed by MF + IFN- or by MF + PT drive Th1 cells via high IL-12
production upon CD40 ligation (T cell engagement). Although poly(I:C)
induces high levels of IL-12 in sentinel myeloid DC (1)
(E. C. de Jong, J. H. N. Schuitemaker, and M. L. Kapsenberg,
unpublished observations), when present during maturation it does not
prime for high IL-12 production. Instead, poly(I:C)-primed DC1s drive
Th1 cells via an unknown soluble factor. Poly(I:C) is used as a model
Ag for viral infections. The relatively low importance of IL-12 in
response to poly(I:C) is in accordance with the finding by Schijns et
al. (24) that IL-12p40/p70-deficient mice still mount
potent Th1 responses upon infection with mouse hepatitis virus and the
finding that patients with a functional mutation of the IL-12R suffer
from infections by various endosomal microorganisms, but not by viruses
(25). Liu and coworkers (26) showed that
plasmacytoid DCs activated with influenza virus promote the development
of Th1 cells via IFN-. Surprisingly, in myeloid DCs the unknown
soluble Th1-driving factor secreted by poly(I:C)-matured DCs is
probably not a type I IFN or IL-18. It is also unlikely to be IL-23
because its p40 subunit is not up-regulated in these DCs (data not
shown) and polyclonal Abs directed against IL-12 only partially inhibit
the Th1-inducing capacity.
Within the DC2s, two types were identified. Although all DC2s express OX40L, only SEA-primed DCs use OX40L to promote the development of Th2 cells. The CT- and PGE2-primed DCs promote Th2 cells via an unidentified soluble factor that is absent in the SEA-primed cells. Possible candidates for the DC-derived Th2-inducing molecules like IL-4, IL-13, PGE2, or monocyte chemoattractant protein-1 do not appear to be involved, because they were not produced at detectable levels and neutralization of their activity had no effect. The identification of this factor(s) is an issue of current investigation.
The heterogeneity of effector DCs and, therefore, of signal 3 reflects the different ways in which various microbial compounds or mediators can activate the sentinel DCs. So far, little is known about the molecular cross-talk between DCs and pathogens. The capability of CT and PGE2 to prime for DC2s can be attributed to their ability to enhance the levels of intracellular cAMP, which block the development of IL-12 responses (27). CT signaling, however, differs from PGE2 signaling in that PGE2 by itself is unable to induce maturation (11), whereas CT does induce maturation (4), although not always completely (data not shown). The different mechanisms by which CT and PGE2 on the one hand and SEA on the other hand prime for DC2s are underscored by the finding that SEA barely up-regulated intracellular cAMP (D. van der Kleij and M. Yazdanbakhsh, unpublished observations).
The capability of PT to prime for DC1 with high IL-12 production, as has also been shown previously in mice in vivo (28), may be explained by the inhibition of Gi protein signaling (29). Thus far, it is unknown how polymerized dsRNA (poly(I:C)) activates DCs to mature into effector DC1s. Possibly it signals through a Toll-like receptor, as has been shown for bacterial DNA motifs and Toll-like receptor 9 (30).
Fully matured effector DCs are resistant to repolarization by microbial stimuli (31) or cytokines (12, 20). This implies that effector DCs primed by a certain microbe are not subject to subsequent cross-modulation by the priming abilities of other pathogens, thereby mediating effective immunity to the first encountered pathogen.
The current findings suggest that, analogous to the development of polarized Th cell subsets from a single precursor population, human DCs are guided by the conditions of their maturation to acquire stable polarized functional effector DC1 or DC2 phenotypes. The present study supports the concept that the type of immune response is optimally adapted to the character of the pathogen via the priming of sentinel DCs into effector DC subsets with unexpectedly diverse functional phenotypes and expression of signal 3.
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Footnotes |
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2 Address correspondence and reprint requests to Dr. Esther C. de Jong, Department of Cell Biology and Histology, Academic Medical Center, University of Amsterdam, P.O. Box 22700, 1100 DE Amsterdam, The Netherlands. E-mail address: E.C.deJong{at}AMC.UvA.NL
3 Abbreviations used in this paper: DC, dendritic cell; OX40L, OX40 ligand; SEA, soluble egg Ags; CT, cholera toxin; PT, pertussis toxin; SEB, Staphylococcus enterotoxin B; CD40L, CD40 ligand; MF, maturation-inducing factors.
Received for publication August 9, 2001. Accepted for publication December 10, 2001.
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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and to bacterial IL-12 inducers: decreased ability of mature dendritic cells to produce IL-12 during the interaction with Th cells. J. Immunol. 162:3231./-producing cells link innate and adaptive immunity. J. Exp. Med. 192:219.This article has been cited by other articles:
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 M. Stasiolek, A. Bayas, N. Kruse, A. Wieczarkowiecz, K. V. Toyka, R. Gold, and K. Selmaj Impaired maturation and altered regulatory function of plasmacytoid dendritic cells in multiple sclerosis Brain, May 1, 2006; 129(5): 1293 - 1305. [Abstract] [Full Text] [PDF]
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 L. O'Mahony, L. O'Callaghan, J. McCarthy, D. Shilling, P. Scully, S. Sibartie, E. Kavanagh, W. O. Kirwan, H. P. Redmond, J. K. Collins, et al. Differential cytokine response from dendritic cells to commensal and pathogenic bacteria in different lymphoid compartments in humans Am J Physiol Gastrointest Liver Physiol, April 1, 2006; 290(4): G839 - G845. [Abstract] [Full Text] [PDF]
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 B. Rethi, P. Gogolak, I. Szatmari, A. Veres, E. Erdos, L. Nagy, E. Rajnavolgyi, C. Terhorst, and A. Lanyi SLAM/SLAM interactions inhibit CD40-induced production of inflammatory cytokines in monocyte-derived dendritic cells Blood, April 1, 2006; 107(7): 2821 - 2829. [Abstract] [Full Text] [PDF]
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C.-C. Chen, S. Louie, B. A. McCormick, W. A. Walker, and H. N. Shi Helminth-Primed Dendritic Cells Alter the Host Response to Enteric Bacterial Infection J. Immunol., January 1, 2006; 176(1): 472 - 483. [Abstract] [Full Text] [PDF]
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A. Skowera, E. C. de Jong, J. H. N. Schuitemaker, J. S. Allen, S. C. Wessely, G. Griffiths, M. Kapsenberg, and M. Peakman Analysis of Anthrax and Plague Biowarfare Vaccine Interactions with Human Monocyte-Derived Dendritic Cells J. Immunol., December 1, 2005; 175(11): 7235 - 7243. [Abstract] [Full Text] [PDF]
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P. M. A. de Graaff, E. C. de Jong, T. M. van Capel, M. E. A. van Dijk, P. J. M. Roholl, J. Boes, W. Luytjes, J. L. L. Kimpen, and G. M. van Bleek Respiratory Syncytial Virus Infection of Monocyte-Derived Dendritic Cells Decreases Their Capacity to Activate CD4 T Cells J. Immunol., November 1, 2005; 175(9): 5904 - 5911. [Abstract] [Full Text] [PDF]
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W. Shen, R. Falahati, R. Stark, D. Leitenberg, and S. Ladisch Modulation of CD4 Th Cell Differentiation by Ganglioside GD1a In Vitro J. Immunol., October 15, 2005; 175(8): 4927 - 4934. [Abstract] [Full Text] [PDF]
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M. Zakharova and H. K. Ziegler Paradoxical Anti-Inflammatory Actions of TNF-{alpha}: Inhibition of IL-12 and IL-23 via TNF Receptor 1 in Macrophages and Dendritic Cells J. Immunol., October 15, 2005; 175(8): 5024 - 5033. [Abstract] [Full Text] [PDF]
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 M. Feili-Hariri, D. H. Falkner, and P. A. Morel Polarization of naive T cells into Th1 or Th2 by distinct cytokine-driven murine dendritic cell populations: implications for immunotherapy J. Leukoc. Biol., September 1, 2005; 78(3): 656 - 664. [Abstract] [Full Text] [PDF]
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D. McIlroy, S. Tanguy-Royer, N. Le Meur, I. Guisle, P.-J. Royer, J. Leger, K. Meflah, and M. Gregoire Profiling dendritic cell maturation with dedicated microarrays J. Leukoc. Biol., September 1, 2005; 78(3): 794 - 803. [Abstract] [Full Text] [PDF]
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A. C. Renkl, J. Wussler, T. Ahrens, K. Thoma, S. Kon, T. Uede, S. F. Martin, J. C. Simon, and J. M. Weiss Osteopontin functionally activates dendritic cells and induces their differentiation toward a Th1-polarizing phenotype Blood, August 1, 2005; 106(3): 946 - 955. [Abstract] [Full Text] [PDF]
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M. Cumberbatch, K. Clelland, R. J. Dearman, and I. Kimber Impact of Cutaneous IL-10 on Resident Epidermal Langerhans' Cells and the Development of Polarized Immune Responses J. Immunol., July 1, 2005; 175(1): 43 - 50. [Abstract] [Full Text] [PDF]
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 P. S. Patole, H.-J. Grone, S. Segerer, R. Ciubar, E. Belemezova, A. Henger, M. Kretzler, D. Schlondorff, and H.-J. Anders Viral Double-Stranded RNA Aggravates Lupus Nephritis through Toll-Like Receptor 3 on Glomerular Mesangial Cells and Antigen-Presenting Cells J. Am. Soc. Nephrol., May 1, 2005; 16(5): 1326 - 1338. [Abstract] [Full Text] [PDF]
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 F. Groot, T. B. H. Geijtenbeek, R. W. Sanders, C. E. Baldwin, M. Sanchez-Hernandez, R. Floris, Y. van Kooyk, E. C. de Jong, and B. Berkhout Lactoferrin Prevents Dendritic Cell-Mediated Human Immunodeficiency Virus Type 1 Transmission by Blocking the DC-SIGN--gp120 Interaction J. Virol., March 1, 2005; 79(5): 3009 - 3015. [Abstract] [Full Text] [PDF]
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B. Pulendran Variegation of the Immune Response with Dendritic Cells and Pathogen Recognition Receptors J. Immunol., March 1, 2005; 174(5): 2457 - 2465. [Abstract] [Full Text] [PDF]
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S. J. Jenkins and A. P. Mountford Dendritic Cells Activated with Products Released by Schistosome Larvae Drive Th2-Type Immune Responses, Which Can Be Inhibited by Manipulation of CD40 Costimulation Infect. Immun., January 1, 2005; 73(1): 395 - 402. [Abstract] [Full Text] [PDF]
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R. Varela-Calvino, A. Skowera, S. Arif, and M. Peakman Identification of a Naturally Processed Cytotoxic CD8 T-Cell Epitope of Coxsackievirus B4, Presented by HLA-A2.1 and Located in the PEVKEK Region of the P2C Nonstructural Protein J. Virol., December 15, 2004; 78(24): 13399 - 13408. [Abstract] [Full Text] [PDF]
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C. M. Kane, L. Cervi, J. Sun, A. S. McKee, K. S. Masek, S. Shapira, C. A. Hunter, and E. J. Pearce Helminth Antigens Modulate TLR-Initiated Dendritic Cell Activation J. Immunol., December 15, 2004; 173(12): 7454 - 7461. [Abstract] [Full Text] [PDF]
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I. M. Klagge, M. Abt, B. Fries, and S. Schneider-Schaulies Impact of measles virus dendritic-cell infection on Th-cell polarization in vitro J. Gen. Virol., November 1, 2004; 85(11): 3239 - 3247. [Abstract] [Full Text] [PDF]
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H. Kuipers, C. Heirman, D. Hijdra, F. Muskens, M. Willart, S. van Meirvenne, K. Thielemans, H. C. Hoogsteden, and B. N. Lambrecht Dendritic cells retrovirally overexpressing IL-12 induce strong Th1 responses to inhaled antigen in the lung but fail to revert established Th2 sensitization J. Leukoc. Biol., November 1, 2004; 76(5): 1028 - 1038. [Abstract] [Full Text] [PDF]
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 R. B. Mailliard, A. Wankowicz-Kalinska, Q. Cai, A. Wesa, C. M. Hilkens, M. L. Kapsenberg, J. M. Kirkwood, W. J. Storkus, and P. Kalinski {alpha}-Type-1 Polarized Dendritic Cells: A Novel Immunization Tool with Optimized CTL-inducing Activity Cancer Res., September 1, 2004; 64(17): 5934 - 5937. [Abstract] [Full Text] [PDF]
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D. Jankovic, M. C. Kullberg, P. Caspar, and A. Sher Parasite-Induced Th2 Polarization Is Associated with Down-Regulated Dendritic Cell Responsiveness to Th1 Stimuli and a Transient Delay in T Lymphocyte Cycling J. Immunol., August 15, 2004; 173(4): 2419 - 2427. [Abstract] [Full Text] [PDF]
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L. Wassink, P. L. Vieira, H. H. Smits, G. A. Kingsbury, A. J. Coyle, M. L. Kapsenberg, and E. A. Wierenga ICOS Expression by Activated Human Th Cells Is Enhanced by IL-12 and IL-23: Increased ICOS Expression Enhances the Effector Function of Both Th1 and Th2 Cells J. Immunol., August 1, 2004; 173(3): 1779 - 1786. [Abstract] [Full Text] [PDF]
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S. L. Young, M. A. Simon, M. A. Baird, G. W. Tannock, R. Bibiloni, K. Spencely, J. M. Lane, P. Fitzharris, J. Crane, I. Town, et al. Bifidobacterial Species Differentially Affect Expression of Cell Surface Markers and Cytokines of Dendritic Cells Harvested from Cord Blood Clin. Vaccine Immunol., July 1, 2004; 11(4): 686 - 690. [Abstract] [Full Text]
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M. Drakes, T. Blanchard, and S. Czinn Bacterial Probiotic Modulation of Dendritic Cells Infect. Immun., June 1, 2004; 72(6): 3299 - 3309. [Abstract] [Full Text] [PDF]
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H. Weigt, P. F. Muhlradt, M. Larbig, N. Krug, and A. Braun The Toll-Like Receptor-2/6 Agonist Macrophage-Activating Lipopeptide-2 Cooperates with IFN-{gamma} to Reverse the Th2 Skew in an In Vitro Allergy Model J. Immunol., May 15, 2004; 172(10): 6080 - 6086. [Abstract] [Full Text] [PDF]
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J. R. Ramirez-Pineda, A. Frohlich, C. Berberich, and H. Moll Dendritic Cells (DC) Activated by CpG DNA Ex Vivo Are Potent Inducers of Host Resistance to an Intracellular Pathogen That Is Independent of IL-12 Derived from the Immunizing DC J. Immunol., May 15, 2004; 172(10): 6281 - 6289. [Abstract] [Full Text] [PDF]
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E. C. Lavelle, A. Jarnicki, E. McNeela, M. E. Armstrong, S. C. Higgins, O. Leavy, and K. H. G. Mills Effects of cholera toxin on innate and adaptive immunity and its application as an immunomodulatory agent J. Leukoc. Biol., May 1, 2004; 75(5): 756 - 763. [Abstract] [Full Text] [PDF]
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A. Mazzoni and D. M. Segal Controlling the Toll road to dendritic cell polarization J. Leukoc. Biol., May 1, 2004; 75(5): 721 - 730. [Abstract] [Full Text] [PDF]
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R. Rouas, P. Lewalle, F. El Ouriaghli, B. Nowak, H. Duvillier, and P. Martiat Poly(I:C) used for human dendritic cell maturation preserves their ability to secondarily secrete bioactive IL-12 Int. Immunol., May 1, 2004; 16(5): 767 - 773. [Abstract] [Full Text] [PDF]
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P. Bjorck Dendritic Cells Exposed to Herpes Simplex Virus In Vivo Do Not Produce IFN-{alpha} after Rechallenge with Virus In Vitro and Exhibit Decreased T Cell Alloreactivity J. Immunol., May 1, 2004; 172(9): 5396 - 5404. [Abstract] [Full Text] [PDF]
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T. Ito, R. Amakawa, M. Inaba, T. Hori, M. Ota, K. Nakamura, M. Takebayashi, M. Miyaji, T. Yoshimura, K. Inaba, et al. Plasmacytoid Dendritic Cells Regulate Th Cell Responses through OX40 Ligand and Type I IFNs J. Immunol., April 1, 2004; 172(7): 4253 - 4259. [Abstract] [Full Text] [PDF]
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P. J. Ross, E. C. Lavelle, K. H. G. Mills, and A. P. Boyd Adenylate Cyclase Toxin from Bordetella pertussis Synergizes with Lipopolysaccharide To Promote Innate Interleukin-10 Production and Enhances the Induction of Th2 and Regulatory T Cells Infect. Immun., March 1, 2004; 72(3): 1568 - 1579. [Abstract] [Full Text] [PDF]
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 C. Teuscher, M. E. Poynter, H. Offner, A. Zamora, T. Watanabe, P. D. Fillmore, J. F. Zachary, and E. P. Blankenhorn Attenuation of Th1 Effector Cell Responses and Susceptibility to Experimental Allergic Encephalomyelitis in Histamine H2 Receptor Knockout Mice Is Due to Dysregulation of Cytokine Production by Antigen-Presenting Cells Am. J. Pathol., March 1, 2004; 164(3): 883 - 892. [Abstract] [Full Text] [PDF]
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F. Trottein, N. Pavelka, C. Vizzardelli, V. Angeli, C. S. Zouain, M. Pelizzola, M. Capozzoli, M. Urbano, M. Capron, F. Belardelli, et al. A Type I IFN-Dependent Pathway Induced by Schistosoma mansoni Eggs in Mouse Myeloid Dendritic Cells Generates an Inflammatory Signature J. Immunol., March 1, 2004; 172(5): 3011 - 3017. [Abstract] [Full Text] [PDF]
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D. J. Davidson, A. J. Currie, G. S. D. Reid, D. M. E. Bowdish, K. L. MacDonald, R. C. Ma, R. E. W. Hancock, and D. P. Speert The Cationic Antimicrobial Peptide LL-37 Modulates Dendritic Cell Differentiation and Dendritic Cell-Induced T Cell Polarization J. Immunol., January 15, 2004; 172(2): 1146 - 1156. [Abstract] [Full Text] [PDF]
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A. Kaser, S. Kaser, N. C. Kaneider, B. Enrich, C. J. Wiedermann, and H. Tilg Interleukin-18 attracts plasmacytoid dendritic cells (DC2s) and promotes Th1 induction by DC2s through IL-18 receptor expression Blood, January 15, 2004; 103(2): 648 - 655. [Abstract] [Full Text] [PDF]
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G. Romagnoli, R. Nisini, P. Chiani, S. Mariotti, R. Teloni, A. Cassone, and A. Torosantucci The interaction of human dendritic cells with yeast and germ-tube forms of Candida albicans leads to efficient fungal processing, dendritic cell maturation, and acquisition of a Th1 response-promoting function J. Leukoc. Biol., January 1, 2004; 75(1): 117 - 126. [Abstract] [Full Text] [PDF]
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 G. Pynaert, P. Rottiers, A. Haegeman, S. Sehra, T. Van Belle, J. Korf, and J. Grooten Antigen Presentation by Local Macrophages Promotes Nonallergic Airway Responses in Sensitized Mice Am. J. Respir. Cell Mol. Biol., November 1, 2003; 29(5): 634 - 641. [Abstract] [Full Text]
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T. Al-Bader, M. Christodoulides, J. E. Heckels, J. Holloway, A. E. Semper, and P. S. Friedmann Activation of Human Dendritic Cells Is Modulated by Components of the Outer Membranes of Neisseria meningitidis Infect. Immun., October 1, 2003; 71(10): 5590 - 5597. [Abstract] [Full Text] [PDF]
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J. C. Gallego-Gomez, C. Risco, D. Rodriguez, P. Cabezas, S. Guerra, J. L. Carrascosa, and M. Esteban Differences in Virus-Induced Cell Morphology and in Virus Maturation between MVA and Other Strains (WR, Ankara, and NYCBH) of Vaccinia Virus in Infected Human Cells J. Virol., October 1, 2003; 77(19): 10606 - 10622. [Abstract] [Full Text] [PDF]
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T. Tatsumi, J. Huang, W. E. Gooding, A. Gambotto, P. D. Robbins, N. L. Vujanovic, S. M. Alber, S. C. Watkins, H. Okada, and W. J. Storkus Intratumoral Delivery of Dendritic Cells Engineered to Secrete Both Interleukin (IL)-12 and IL-18 Effectively Treats Local and Distant Disease in Association with Broadly Reactive Tc1-type Immunity Cancer Res., October 1, 2003; 63(19): 6378 - 6386. [Abstract] [Full Text] [PDF]
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 A J Stagg, A L Hart, S C Knight, and M A Kamm The dendritic cell: its role in intestinal inflammation and relationship with gut bacteria Gut, October 1, 2003; 52(10): 1522 - 1529. [Abstract] [Full Text] [PDF]
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H. Kuipers, D. Hijdra, V. C. de Vries, H. Hammad, J.-B. Prins, A. J. Coyle, H. C. Hoogsteden, and B. N. Lambrecht Lipopolysaccharide-Induced Suppression of Airway Th2 Responses Does Not Require IL-12 Production by Dendritic Cells J. Immunol., October 1, 2003; 171(7): 3645 - 3654. [Abstract] [Full Text] [PDF]
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S. Xu, G. K. Koski, M. Faries, I. Bedrosian, R. Mick, M. Maeurer, M. A. Cheever, P. A. Cohen, and B. J. Czerniecki Rapid High Efficiency Sensitization of CD8+ T Cells to Tumor Antigens by Dendritic Cells Leads to Enhanced Functional Avidity and Direct Tumor Recognition Through an IL-12-Dependent Mechanism J. Immunol., September 1, 2003; 171(5): 2251 - 2261. [Abstract] [Full Text] [PDF]
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E. C. Lavelle, E. McNeela, M. E. Armstrong, O. Leavy, S. C. Higgins, and K. H. G. Mills Cholera Toxin Promotes the Induction of Regulatory T Cells Specific for Bystander Antigens by Modulating Dendritic Cell Activation J. Immunol., September 1, 2003; 171(5): 2384 - 2392. [Abstract] [Full Text] [PDF]
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W. Hou, Y. Wu, S. Sun, M. Shi, Y. Sun, C. Yang, G. Pei, Y. Gu, C. Zhong, and B. Sun Pertussis Toxin Enhances Th1 Responses by Stimulation of Dendritic Cells J. Immunol., February 15, 2003; 170(4): 1728 - 1736. [Abstract] [Full Text] [PDF]
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M. Jinushi, T. Takehara, T. Kanto, T. Tatsumi, V. Groh, T. Spies, T. Miyagi, T. Suzuki, Y. Sasaki, and N. Hayashi Critical Role of MHC Class I-Related Chain A and B Expression on IFN-{alpha}-Stimulated Dendritic Cells in NK Cell Activation: Impairment in Chronic Hepatitis C Virus Infection J. Immunol., February 1, 2003; 170(3): 1249 - 1256. [Abstract] [Full Text] [PDF]
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A. D. Straw, A. S. MacDonald, E. Y. Denkers, and E. J. Pearce CD154 Plays a Central Role in Regulating Dendritic Cell Activation During Infections That Induce Th1 or Th2 Responses J. Immunol., January 15, 2003; 170(2): 727 - 734. [Abstract] [Full Text] [PDF]
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A. Boonstra, C. Asselin-Paturel, M. Gilliet, C. Crain, G. Trinchieri, Y.-J. Liu, and A. O'Garra Flexibility of Mouse Classical and Plasmacytoid-derived Dendritic Cells in Directing T Helper Type 1 and 2 Cell Development: Dependency on Antigen Dose and Differential Toll-like Receptor Ligation J. Exp. Med., January 6, 2003; 197(1): 101 - 109. [Abstract] [Full Text] [PDF]
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D. Sewell, Z. Qing, E. Reinke, D. Elliot, J. Weinstock, M. Sandor, and Z. Fabry Immunomodulation of experimental autoimmune encephalomyelitis by helminth ova immunization Int. Immunol., January 1, 2003; 15(1): 59 - 69. [Abstract] [Full Text] [PDF]
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 D. van der Kleij, E. Latz, J. F. H. M. Brouwers, Y. C. M. Kruize, M. Schmitz, E. A. Kurt-Jones, T. Espevik, E. C. de Jong, M. L. Kapsenberg, D. T. Golenbock, et al. A Novel Host-Parasite Lipid Cross-talk. SCHISTOSOMAL LYSO-PHOSPHATIDYLSERINE ACTIVATES TOLL-LIKE RECEPTOR 2 AND AFFECTS IMMUNE POLARIZATION J. Biol. Chem., December 6, 2002; 277(50): 48122 - 48129. [Abstract] [Full Text] [PDF]
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A. D. Edwards, S. P. Manickasingham, R. Sporri, S. S. Diebold, O. Schulz, A. Sher, T. Kaisho, S. Akira, and C. Reis e Sousa Microbial Recognition Via Toll-Like Receptor-Dependent and -Independent Pathways Determines the Cytokine Response of Murine Dendritic Cell Subsets to CD40 Triggering J. Immunol., October 1, 2002; 169(7): 3652 - 3660. [Abstract] [Full Text] [PDF]
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T. Tatsumi, L. S. Kierstead, E. Ranieri, L. Gesualdo, F. P. Schena, J. H. Finke, R. M. Bukowski, J. Mueller-Berghaus, J. M. Kirkwood, W. W. Kwok, et al. Disease-associated Bias in T Helper Type 1 (Th1)/Th2 CD4+ T Cell Responses Against MAGE-6 in HLA-DRB10401+ Patients With Renal Cell Carcinoma or Melanoma J. Exp. Med., September 2, 2002; 196(5): 619 - 628. [Abstract] [Full Text] [PDF]
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R. W. Sanders, E. C. de Jong, C. E. Baldwin, J. H. N. Schuitemaker, M. L. Kapsenberg, and B. Berkhout Differential Transmission of Human Immunodeficiency Virus Type 1 by Distinct Subsets of Effector Dendritic Cells J. Virol., June 27, 2002; 76(15): 7812 - 7821. [Abstract] [Full Text] [PDF]
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S. Ebner, S. Hofer, V. A. Nguyen, C. Furhapter, M. Herold, P. Fritsch, C. Heufler, and N. Romani A Novel Role for IL-3: Human Monocytes Cultured in the Presence of IL-3 and IL-4 Differentiate into Dendritic Cells That Produce Less IL-12 and Shift Th Cell Responses Toward a Th2 Cytokine Pattern J. Immunol., June 15, 2002; 168(12): 6199 - 6207. [Abstract] [Full Text] [PDF]
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 M. Yazdanbakhsh, P. G. Kremsner, and R. van Ree Allergy, Parasites, and the Hygiene Hypothesis Science, April 19, 2002; 296(5567): 490 - 494. [Abstract] [Full Text] [PDF]
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