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Center for Immunology, University of Minnesota, Minneapolis, MN 55455
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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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or IL-1 3 . The effects of these may
be related, because TNF- induces IL-1 production 4 . Thus, these
inflammatory cytokines are necessary and sufficient to support the
response in the absence of other adjuvants.
Where and how the inflammatory cytokines act to promote T cell
responses is less clear. Studies of CD4+ T cell lines
suggest that IL-1 may contribute to activation through direct
interaction with the T cell 5, 6, 7, 8 . Alternatively, the cytokines may
act indirectly by up-regulating, on APCs, the expression of ligands
that costimulate T cell activation 9 . TNF- and IL-1 can induce the
expression of CD40 on dendritic cells 10 and CD40-dependent signaling
can in turn increase B7 expression on APC 11, 12, 13 , thus increasing the
level of costimulation available to the T cells. Proliferation and
differentiation of CD8+ T cells to generate cytotoxic T
lymphocyte responses can also be enhanced by inflammatory cytokines
produced by macrophages and/or dendritic cells, cytokines that include
IL-1 14 , IL-6 14, 15 , IL-12 16, 17, 18 , and IFN-
19 . Like
CD4+ T cells, it is unclear whether these cytokines act
directly on the CD8+ T cells, or indirectly by enhancing Ag
presentation or costimulation by APC.
MHC protein/peptide Ag complexes immobilized on inert microspheres can be used to study T cell activation requirements in the absence of APC 20 , thus making it possible to determine whether inflammatory cytokines have a direct effect on the T cells. Using this approach with highly purified naive T cells from TCR transgenic mice and signal 2 provided in the form of either exogenous IL-2 or coimmobilized B7.1 protein 21 , we found that IL-1 significantly enhanced the response of CD4+ T cells, whereas IL-12 was required for a response by CD8+ T cells. The latter finding predicted that IL-12 may act as an effective adjuvant for in vivo induction of a CD8+ T cell response, and this prediction was confirmed. Many aspects of T cell activation can be accounted for by a two-signal model 22 with signal 1 provided by the TCR and signal 2 by costimulation leading to IL-2 production 23, 24, 25 . The results described in this report suggest that a three signal model may more adequately describe T cell activation requirements, with the third signal being a "danger signal" provided by an inflammatory cytokine, IL-1 in the case of CD4+ T cells and IL-12 in the case of CD8+ T cells, that acts directly on the T cell.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Lymph node (LN)3 cells from OT-I mice 26 were harvested and passed over Cellect-plus CD8 enrichment columns (Biotex Laboratories, Edmonton, Alberta, Canada). The cells were then stained with anti-CD44-FITC and anti-CD8-phycoerythrin mAbs and sorted using a FACSvantage flow cytometer (Becton Dickinson, Mansfield, MA) to obtain a population of naive CD8+ CD44low cells (>98% CD44low). LN and spleen cells were harvested from DO11.10 mice 27 , depleted of adherent cells by incubation on plastic petri dishes for 1 h, and passed over Cellect-plus CD4 enrichment columns. The cells were then stained with anti-CD45RB-FITC mAb and sorted to obtain naive CD4+CD45RBhigh cells (>98% CD45RBhigh).
Proliferation and cytotoxicity assays
A total of 5 x 104 purified T cells and 105 Ag-coated latex microspheres were placed in flat-bottom microtiter wells in 200 µl of RPMI 1640 medium supplemented with 10% FCS, 4 mM L-glutamine, 0.1 mM nonessential amino acids, 1 mM sodium pyruvate, 100 U/ml penicillin and streptomycin, 10 mM HEPES, and 5 µM 2-ME. Where indicated, cultures were supplemented with human rIL-2 (R&D Systems, Minneapolis, MN), mouse rIL-12 (Genetics Institute, Cambridge, MA), or mouse rIL-1ß (R&D Systems). Proliferation was measured after 3 days for CD8+ T cells and after 4 days for CD4+ T cells by addition of 1 µCi [3H]TdR per well for the last 8 h of culture. In some experiments, neutralizing antiserum against IL-12 (sheep anti-mouse IL-12; Genetics Institute) or mAb to IL-1R (PharMingen, San Diego, CA) were used. Triplicate determinations were done, and SDs are shown. Cytolytic activity was determined in a standard 4-h 51Cr release assay using E.G7 cells (EL4 cells transfected with OVA) as targets, with EL4 cells included as a control for specificity.
Ags on microspheres
H-2Kb was purified, incorporated onto 5-micron-diameter latex microspheres and pulsed with OVA257–264 as previously described 20 using 3.5 µg H-2Kb per 107 beads for immobilization. Peptide pulsing was done using 2 µM peptide, unless otherwise indicated. IAd/OVA327–339 fusion protein 28 was obtained from L cells transfected with a full-length construct that included the cyoplasmic and transmembrane regions of the class II protein. These cells were a kind gift from Dr. Andrea J. Sant (University of Chicago, Chicago, IL). Cells were solubilized using Triton X-100, and the IAd/OVA327–339 protein was purified by affinity chromatography using M5/114 mAb specific for IAßd. The purified protein was incorporated onto latex microspheres exactly as for H-2Kb 20 , and the extent of immobilization determined by flow cytometry using the M5/114 mAb. Native B7.1 protein was purified by affinity chromatography and immobilized on microspheres as previously described 21, 29 . For all microsphere preparations, the surface density of immobilized B7.1 was determined by flow cytometry to insure that it was in the range previously shown to provide effective costimulation to T cells 21 .
Adoptive transfer and immunization
LN cells were harvested from 2C TCR transgenic mice 30 , labeled with the fluorescent dye PKH26-GL (Sigma, St. Louis, MO) according to the supplier’s protocol and adoptively transferred into C57BL/6 mice (Charles River Laboratory, Wilmington, MA) by suspending 3–4 x 106 CD8+ cells in 0.5 ml PBS and injecting into the tail vein. After transfer, mice were rested for 1 day and then immunized (day 0) by s.c. injection of a total of 0.3 ml Ag in two sites on the back. Ag was SIYRYYGL peptide 31 in either PBS or emulsified in CFA. Cytokines were administered i.p. in 0.1 ml doses on days 0, 1, and 2. IL-12 was administered at 1 µg/day in PBS with 1% mouse serum, and IL-1ß was administered at 0.5 µg/day in PBS with 0.1% BSA. On day 3, mice were sacrificed, and cells from draining LN, spleen and peripheral blood were analyzed by flow cytometry to determine the total number of 2C cells and their PKH26-GL fluorescence. 2C cells were identified by staining with 1B2 mAb specific for the TCR (Ref. 32; a gift from Dr. H. Eisen) and anti-CD8 mAb. These methods for identification, enumeration, and phenotypic characterization of adoptively transferred 2C cells, have been described in detail 33 .
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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Naive (CD44low) CD8+ T cells were purified
by FACS from OT-I mice having a transgenic TCR specific for
OVA257–264 peptide and H-2Kb 26 to yield a
population having >99% CD8+CD44low T cells
(Fig. 1
) that are >99% positive for the
V2 transgenic TCR. The purified cells are Ly-6C-,
CD25-, and CD69- and have the forward scatter
profile of small resting lymphocytes, consistent with being naive cells
(data not shown). Artificial APC were prepared by immobilizing
H-2Kb on latex microspheres and pulsing with
OVA257–264 to form Ag complexes. Beads prepared in this
way stimulate strong Ag-specific proliferation of CD44high
memory cells from OT-I mice, provided that exogenous IL-2 is added
20 . In contrast, naive CD44low cells respond only
marginally to beads and IL-2 (Ref. 20 and Fig. 2A). However, Ag and IL-2
stimulate vigorous proliferation of naive cells when IL-12 is also
added (Fig. 2A). The response depends on all three stimuli
(Fig. 2A), and addition of anti-IL-2 mAb to the cultures
blocks the response in the presence of IL-12 (data not shown).
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B). To determine whether the requirement for
three stimuli might be resulting from suboptimal amounts of one of the
stimuli, the concentration dependence for each was measured.
Proliferation as a function of the concentrations of peptide complex
(Fig. 3A), IL-12 (Fig. 3B), or IL-2 (Fig. 3C) were determined with the
other two stimuli held constant. In all cases, proliferation remained
completely dependent on the presence of all three stimuli over the
effective concentration ranges of each of the stimuli. In the absence
of IL-2, IL-12 alone did not support a response to Ag even at high
concentrations (Fig. 3B) and IL-12 did not enhance survival
of unstimulated CD8+ T cells (data not shown).
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Although IL-12 acts synergistically with Ag and IL-2 in
stimulating CD8+ T cells, other inflammatory cytokines
including IL-1, IL-6, and TNF- did not support the response (data
not shown). This finding was somewhat surprising because IL-1 can
replace adjuvant in supporting Ag-dependent in vivo clonal expansion of
CD4+ T cells 3 , whereas IL-12 promotes differentiation to
a Th1 phenotype 3, 34 but has little effect on the extent of clonal
expansion. These results predicted that CD4+ cells may
respond differently than CD8+ cells to inflammatory
cytokines in vitro; therefore, experiments were done to compare the two
cell types. The response of CD8+ T cells to Ag and IL-2 was
not increased by the addition of IL-1ß, whereas IL-12 supported
vigorous proliferation, and this response was blocked by addition of
anti-IL-12 Ab (Fig. 4A).
The CD4+ response was examined using naive
(CD45Rbhigh) CD4+ T cells from D011.10 TCR
transgenic mice 27 and artificial APC made using
I-Ad/OVA327–339 fusion protein 28 . Ag alone
induced a weak proliferative response that was increased about 2-fold
when either IL-2 or IL-1ß was added, and addition of both gave the
strongest response (Fig. 4B). All three components were
required for maximal response (Fig. 4B), and the response
was completely blocked by anti-IL-2R mAb (data not shown). In
contrast to IL-1, IL-12 had no effect on the CD4+ T cell
response to Ag or Ag plus IL-2 (Fig. 4B). Thus, responses of
naive CD4+ T cells are enhanced by IL-1 but not IL-12,
whereas responses of naive CD8+ T cells require IL-12 but
not IL-1.
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To determine whether the B7.1 costimulatory ligand may alter the
requirements for inflammatory cytokines, microspheres having Ag and
purified B7.1 coimmobilized on the same surface were prepared and used
to stimulate cells. B7.1 was immobilized at a surface density
previously shown to yield effective costimulation along with
anti-TCR mAb 21 , and this density was confirmed by flow cytometry
21, 29 . The presence of the B7.1 on the same surface as the
H-2Kb/OVA257–264 Ag did not eliminate a
requirement for IL-12 in stimulating OT-1 cells (Fig. 4C).
CD8+ cells make low levels of IL-2, and optimal
proliferation required the addition of exogenous IL-2 even when B7.1
was present; biological activity of the B7.1 was confirmed in
experiments examining CD4+ cells. When Ag and B7.1 were
coimmobilized and used to stimulate DO11.10 cells, B7.1-dependent
costimulation caused sufficient IL-2 production to increase the
response over that of Ag alone, and IL-1ß doubled the response (Fig. 4D). Addition of anti-IL-1R mAb decreased the response
to the same level obtained when just Ag/B7.1 beads were used,
confirming that the effects are IL-1-dependent. Again, neither IL-12
(Fig. 4D) nor TNF- (data not shown) enhanced the
CD4+ T cell responses. Thus, when signal 2 is
provided either in the form of IL-2 or IL-2 and B7.1 ligand, naive
CD8+ T cells remain dependent on IL-12 for a strong
proliferative response, whereas IL-1ß substantially increases the
response of CD4+ T cells when either IL-2 or B7.1 ligand
are used to provide signal 2.
IL-12 is required for differentiation of naive CD8+ T cells to lytic effector cells
In addition to proliferating in response to Ag-specific
stimulation, naive CD8+ T cells develop lytic effector
function by day 3. Cytolytic activity of cells cultured with Ag alone
or Ag and IL-12 could not be determined because too few viable cells
remained to be assayed by day 3. A low level of proliferation of OT-1
cells does occur in response to just Ag and IL-2 (
Figs. 2–4), and
sufficient viable cells could be recovered from these cultures on day 3
to determine whether they had acquired lytic activity. Cells stimulated
with Ag and IL-2, or with just IL-2 and IL-12 in the absence of Ag, did
not develop detectable cytolytic activity (Fig. 5). In contrast, cells stimulated with
Ag, IL-2, and IL-12 developed potent Ag-specific cytolytic activity.
Thus, in addition to being required to support optimal proliferation,
both IL-2 and IL-12 are required along with Ag to support acquisition
of lytic effector function by naive cells.
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The in vitro results described above predicted that IL-12 may
replace adjuvant in stimulating an in vivo response of CD8+
cells to peptide. This finding was examined by adoptively transferring
CD8+ T cells from 2C TCR transgenic mice 30 into C57BL/6
recipients, challenging with SIYRYYGL peptide recognized by the 2C
receptor on H-2Kb 31 and assessing the in vivo response
by flow cytometry using 1B2 anti-clonotype mAb and anti-CD8 mAb
to identify 2C cells 33 . A s.c. injection of just peptide caused
minimal clonal expansion in draining lymph nodes or spleen, whereas
peptide in CFA caused a large increase in the number of 2C cells in the
draining nodes (Fig. 6). IL-12 along with
peptide also caused a large increase in 2C cell number, and the
increase was seen in both the draining lymph nodes and spleen. It
appears likely that the Ag depot effect of the mineral oil in CFA
results in the response being limited to the draining lymph nodes,
whereas free peptide readily reaches other sites, including the spleen
in which clonal expansion can occur if IL-12 is present.
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), IL-1ß did not substantially increase the
numbers of 2C cells in the draining nodes or spleen in comparison to
the numbers present in response to just peptide (Fig. 6). In two
independent experiments, peptide and IL-1 caused 6.2- and 7.8-fold
increases in the numbers of 2C cells in comparison with transfer only
mice, whereas in these same experiments, peptide and IL-12 caused 26-
and 40-fold increases. This result is in marked contrast to
CD4+ T cells responses, in which IL-1 supports clonal
expansion comparable with that obtained using CFA, whereas IL-12 does
not 3 .
To ensure that changes in the numbers of 2C cells reflected
proliferation, rather than increased migration into the draining nodes
or spleen, cells were labeled with PKH26 fluorescent dye before
transfer, and PKH26 fluorescence levels were determined on day 3. PKH26
incorporates into the cell membrane, and the fluorescence of the cell
decreases as the dye is diluted upon cell division. Peptide alone
stimulated some cell division, and administration of peptide with
either CFA or IL-12 resulted in more extensive cell division by day 3
(Fig. 7). Less than 10% of 2C cells had
undergone more than four divisions in transfer only mice, <30% in
peptide only mice, and >65% in peptide + IL-12 or peptide + CFA mice.
Although the differences between peptide alone vs peptide along with
IL-12 or CFA do not appear great when these profiles are examined, it
must be kept in mind that relatively small differences in the number of
divisions can result in large differences in the extent of clonal
expansion. Furthermore, the extent of clonal expansion will be also be
influenced by the rate and extent of cell death. Thus, the results
obtained with PKH26 labeling do not provide a useful measure of the
relative efficiencies of the different immunizations in expanding the
2C cell population. However, the results do support the conclusion that
the majority of 2C cells proliferate in response to Ag, even when this
is peptide alone that does not cause large clonal expansion (Fig. 6).
Thus, the increased numbers of 2C cells in the draining LN and spleen
are not simply due to migration.
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Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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), whereas IL-1 augments a CD4
response to Ag and IL-2 (Fig. 4). We recently showed that IL-2 and H-2Kb immobilized on microspheres and pulsed with OVA257–264 peptide were sufficient to stimulate proliferation and development of effector function by memory (CD44high) CD8+ T cells from OT-1 mice 20 . In contrast, naive (CD44low) OT-1 cells showed only marginal proliferation and no development of lytic function in response to these stimuli despite the fact that the naive and memory cells expressed the same TCR and had almost identical surface densities of TCR and CD8. Those observations suggested that the signals needed to activate naive and memory CD8+ T cells differed either quantitatively or qualitatively.
It is clear from the present experiments that IL-12 can supply the
missing signal to the naive cells, and that this is a direct effect of
IL-12 on the T cells (
Figs. 2–5). IL-12 has previously been shown to
enhance CD8+ T cell responses 16, 17, 18 , as have numerous
other cytokines including IL-1 14 , IL-6 14, 15 , IFN- 19 , and
others. However, it has been unclear whether these reflect direct
effects on the CD8+ T cell or effects on APC that enhance
delivery of signal 2 to the T cells. Although IL-12 can supply the
missing signal to naive CD8+ T cells in the absence of APC,
this was not the case for IL-1 (Fig. 4), TNF-, or IL-6 (data not
shown). It also appears that IL-12 is not acting through its ability to
stimulate T cell production of IFN- 35 , because the addition of
anti-IFN- Ab did not block the response to Ag, IL-2, and IL-12
(data not shown). Although only IL-12, of the cytokines tested, was
able to support the CD8 T cell response, it is possible that there is
some redundancy with other cytokines that are also able to support the
response. Redundancy is seen with respect to signal 2 delivery; CD28/B7
seems to be the major pathway but a number of other receptor/ligand
pairs have been implicated as providing costimulatory signals. It may
also be the case that signal 3 is not always required. Signal 1, or
signals 1 and 2, may be sufficient for activation at very high Ag
levels or very high TCR affinity for Ag 37, 38 ; quantitative
differences in signal 1 may determine whether one, two, or three
signals are necessary for full activation. That IL-12 is not always
required for CTL responses is suggested by the fact that cells from
mice deficient in the IL-12 p40 gene and thus unable to make active
IL-12 are still able to generate an allogeneic CTL response 36 .
Similarly, we have found that neutralizing anti-IL-12 mAb is unable
to block proliferation of CD8+ T cells when peptide pulsed
spleen cells are used as APC (data not shown). Experiments are in
progress to determine whether quantitative Ag effects, alternative
cytokines, or both are involved in overcoming a requirement for IL-12
under some circumstances.
These in vitro results predicted that IL-12 may serve as an effective
adjuvant in vivo and were confirmed using an adoptive transfer system
to examine clonal expansion of TCR transgenic CD8+ T cells
from 2C mice (Figs. 6 and 7). A striking parallel was found between the
in vitro and in vivo responses. In the absence of IL-12, a low level of
proliferation occurred in vitro in response to Ag and IL-2 (Figs. 2 and 3). In vivo, clonal expansion was minimal in response to just peptide,
but the 2C cells had clearly recognized and responded to Ag, as
evidenced by that fact that all of the cells recovered from the
draining LN had undergone some proliferation (Fig. 7) and a substantial
fraction (40–50%) had acquired a CD44high phenotype (data
not shown). Addition of IL-12 in vitro resulted in a strong
proliferative response, and in vivo administration along with peptide
resulted in extensive clonal expansion, as good or better than that
obtained using peptide with CFA (Fig. 6). This finding is consistent
with previous reports that IL-12 administration can enhance in vivo CTL
responses 18, 39 and suggests that IL-12 will provide a means for
effectively inducing CD8+ responses when peptide Ags are
used for vaccination or therapy.
The in vitro effects of inflammatory cytokines on the CD4+
cells described here also agreed well with in vivo effects that have
been previously described 3, 34 . Substantial proliferation occurs in
vitro in response to Ag and signal 2 in the form of either
coimmobilized B7.1 or exogenous IL-2 and nearly doubles when IL-1 is
added (Fig. 4). Similarly, in vivo administration of Ag alone results
in substantial B7-dependent clonal expansion 40 , and coadministration
of IL-1 approximately doubles the expansion 3 . TNF- also supports
in vivo Ag-specific clonal expansion. However, it does not enhance the
in vitro response to Ag and signal 2 (data not shown). It probably acts
in vivo by inducing production of IL-1 by APC 4 and is thus inactive
in vitro when APC are not present. In contrast to its effects on
CD8+ T cells, IL-12 does not significantly enhance either
in vitro proliferation or in vivo clonal expansion of CD4+
T cells. However, it does act as an inducer of Th1 differentiation of
CD4+ cells 3, 34, 41 .
In vivo administration of just Ag results in significant clonal
expansion of CD4+ T cells; the Ag-specific cells are
present in expanded numbers but have been rendered tolerant.
Coadministration of adjuvants prevents tolerance induction, as does
coadministration of IL-1 3, 34 . Tolerance of CD8+ T cells
can also result when peptide Ag is administered in the absence of
adjuvant 42 ; proliferation is very limited under these conditions
(Figs. 6 and 7) and preliminary results suggest that this may lead to
clonal deletion (data not shown). Coadministration of IL-12 can reverse
this by supporting strong clonal expansion in response to the Ag (Fig. 6). Thus, for both CD4+ and CD8+ T cells,
inflammatory cytokines produced by APC in response to pathogens can
provide a third signal needed to support optimal proliferation and
avoid tolerizing the cells in response to Ag and signal 2. These
cytokines may well be the predominant signalers of "danger" that
the innate immune system provides to the adaptive immune response 1, 2 . IL-1 will support CD4+ T cell expansion and promote Th2
help for a humoral response. IL-12 will favor a cell-mediated response
by promoting Th1 differentiation of CD4 cells 3, 34, 41 and signaling
for expansion (Fig. 6) and differentiation (Fig. 5) of CD8+
T cells. Differential effects of pathogens on the production of these
two cytokines may have profound effects on the nature of the immune
response that can be generated.
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Acknowledgments |
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Footnotes |
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2 Address correspondence and reprint requests to Dr. Matthew F. Mescher, Center for Immunology, Box 334 Mayo, 420 Delaware St. S.E., Minneapolis, MN 55455. E-mail address:
3 Abbreviation used in this paper: LN, lymph node.
Received for publication August 13, 1998. Accepted for publication December 14, 1998.
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References |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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in vivo. Int. Immunol. 6:157. interferon for their growth and differentiation into effector cells. Curr. Top. Microbiol. Immunol. 126:173.[Medline]
production and type 1 cytokine responses. Immunity 4:471.[Medline]
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K. A. Casey and M. F. Mescher IL-21 Promotes Differentiation of Naive CD8 T Cells to a Unique Effector Phenotype J. Immunol., June 15, 2007; 178(12): 7640 - 7648. [Abstract] [Full Text] [PDF]
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 Z. Xiao, J. M. Curtsinger, M. Prlic, S. C. Jameson, and M. F. Mescher The CD8 T cell response to vaccinia virus exhibits site-dependent heterogeneity of functional responses Int. Immunol., June 1, 2007; 19(6): 733 - 743. [Abstract] [Full Text] [PDF]
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J. M. Curtsinger, M. Y. Gerner, D. C. Lins, and M. F. Mescher Signal 3 Availability Limits the CD8 T Cell Response to a Solid Tumor J. Immunol., June 1, 2007; 178(11): 6752 - 6760. [Abstract] [Full Text] [PDF]
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X. Chen, O. M. Z. Howard, and J. J. Oppenheim Pertussis Toxin by Inducing IL-6 Promotes the Generation of IL-17-Producing CD4 Cells J. Immunol., May 15, 2007; 178(10): 6123 - 6129. [Abstract] [Full Text] [PDF]
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H. Li, S. Nookala, and F. Re Aluminum Hydroxide Adjuvants Activate Caspase-1 and Induce IL-1beta and IL-18 Release J. Immunol., April 15, 2007; 178(8): 5271 - 5276. [Abstract] [Full Text] [PDF]
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S. S. Way, C. Havenar-Daughton, G. A. Kolumam, N. N. Orgun, and K. Murali-Krishna IL-12 and Type-I IFN Synergize for IFN-{gamma} Production by CD4 T Cells, Whereas Neither Are Required for IFN-{gamma} Production by CD8 T Cells after Listeria monocytogenes Infection J. Immunol., April 1, 2007; 178(7): 4498 - 4505. [Abstract] [Full Text] [PDF]
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D. L. Turner, L. S. Cauley, K. M. Khanna, and L. Lefrancois Persistent Antigen Presentation after Acute Vesicular Stomatitis Virus Infection J. Virol., February 15, 2007; 81(4): 2039 - 2046. [Abstract] [Full Text] [PDF]
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 E. M. Coulter, J. Farrell, K. L. Mathews, J. L. Maggs, C. K. Pease, D. J. Lockley, D. A. Basketter, B. K. Park, and D. J. Naisbitt Activation of Human Dendritic Cells by p-Phenylenediamine J. Pharmacol. Exp. Ther., February 1, 2007; 320(2): 885 - 892. [Abstract] [Full Text] [PDF]
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H. M. Tse, M. J. Milton, S. Schreiner, J. L. Profozich, M. Trucco, and J. D. Piganelli Disruption of Innate-Mediated Proinflammatory Cytokine and Reactive Oxygen Species Third Signal Leads to Antigen-Specific Hyporesponsiveness J. Immunol., January 15, 2007; 178(2): 908 - 917. [Abstract] [Full Text] [PDF]
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Y. F. Lau, G. Deliyannis, W. Zeng, A. Mansell, D. C. Jackson, and L. E. Brown Lipid-containing mimetics of natural triggers of innate immunity as CTL-inducing influenza vaccines Int. Immunol., December 1, 2006; 18(12): 1801 - 1813. [Abstract] [Full Text] [PDF]
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 M. Prlic, G. Hernandez-Hoyos, and M. J. Bevan Duration of the initial TCR stimulus controls the magnitude but not functionality of the CD8+ T cell response J. Exp. Med., September 4, 2006; 203(9): 2135 - 2143. [Abstract] [Full Text] [PDF]
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 R. W. Kaminski, K. R. Turbyfill, and E. V. Oaks Mucosal adjuvant properties of the Shigella invasin complex. Infect. Immun., May 1, 2006; 74(5): 2856 - 2866. [Abstract] [Full Text] [PDF]
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C. Havenar-Daughton, G. A. Kolumam, and K. Murali-Krishna Cutting Edge: The Direct Action of Type I IFN on CD4 T Cells Is Critical for Sustaining Clonal Expansion in Response to a Viral but Not a Bacterial Infection J. Immunol., March 15, 2006; 176(6): 3315 - 3319. [Abstract] [Full Text] [PDF]
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J. M. Curtsinger, D. C. Lins, C. M. Johnson, and M. F. Mescher Signal 3 Tolerant CD8 T Cells Degranulate in Response to Antigen but Lack Granzyme B to Mediate Cytolysis J. Immunol., October 1, 2005; 175(7): 4392 - 4399. [Abstract] [Full Text] [PDF]
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A. Audige, E. Schlaepfer, H. Joller, and R. F. Speck Uncoupled Anti-HIV and Immune-Enhancing Effects when Combining IFN-{alpha} and IL-7 J. Immunol., September 15, 2005; 175(6): 3724 - 3736. [Abstract] [Full Text] [PDF]
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M. A. Markiewicz, L. N. Carayannopoulos, O. V. Naidenko, K. Matsui, W. R. Burack, E. L. Wise, D. H. Fremont, P. M. Allen, W. M. Yokoyama, M. Colonna, et al. Costimulation through NKG2D Enhances Murine CD8+ CTL Function: Similarities and Differences between NKG2D and CD28 Costimulation J. Immunol., September 1, 2005; 175(5): 2825 - 2833. [Abstract] [Full Text] [PDF]
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J. Xiang, H. Huang, and Y. Liu A New Dynamic Model of CD8+ T Effector Cell Responses via CD4+ T Helper-Antigen-Presenting Cells J. Immunol., June 15, 2005; 174(12): 7497 - 7505. [Abstract] [Full Text] [PDF]
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A. A. Filatenkov, E. L. Jacovetty, U. B. Fischer, J. M. Curtsinger, M. F. Mescher, and E. Ingulli CD4 T Cell-Dependent Conditioning of Dendritic Cells to Produce IL-12 Results in CD8-Mediated Graft Rejection and Avoidance of Tolerance J. Immunol., June 1, 2005; 174(11): 6909 - 6917. [Abstract] [Full Text] [PDF]
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S. S. Kang and P. M. Allen Priming in the Presence of IL-10 Results in Direct Enhancement of CD8+ T Cell Primary Responses and Inhibition of Secondary Responses J. Immunol., May 1, 2005; 174(9): 5382 - 5389. [Abstract] [Full Text] [PDF]
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J. M. Curtsinger, J. O. Valenzuela, P. Agarwal, D. Lins, and M. F. Mescher Cutting Edge: Type I IFNs Provide a Third Signal to CD8 T Cells to Stimulate Clonal Expansion and Differentiation J. Immunol., April 15, 2005; 174(8): 4465 - 4469. [Abstract] [Full Text] [PDF]
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 J. M. Matheson, V. J. Johnson, V. Vallyathan, and M. I. Luster Exposure and Immunological Determinants in a Murine Model for Toluene Diisocyanate (TDI) Asthma Toxicol. Sci., March 1, 2005; 84(1): 88 - 98. [Abstract] [Full Text] [PDF]
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J. O. Valenzuela, C. D. Hammerbeck, and M. F. Mescher Cutting Edge: Bcl-3 Up-Regulation by Signal 3 Cytokine (IL-12) Prolongs Survival of Antigen-Activated CD8 T Cells J. Immunol., January 15, 2005; 174(2): 600 - 604. [Abstract] [Full Text] [PDF]
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R. M. Johnson Murine Oviduct Epithelial Cell Cytokine Responses to Chlamydia muridarum Infection Include Interleukin-12-p70 Secretion Infect. Immun., July 1, 2004; 72(7): 3951 - 3960. [Abstract] [Full Text] [PDF]
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M. Apostolaki and N. A. Williams Nasal Delivery of Antigen with the B Subunit of Escherichia coli Heat-Labile Enterotoxin Augments Antigen-Specific T-Cell Clonal Expansion and Differentiation Infect. Immun., July 1, 2004; 72(7): 4072 - 4080. [Abstract] [Full Text] [PDF]
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A. Th. den Boer, G. J. D. van Mierlo, M. F. Fransen, C. J. M. Melief, R. Offringa, and R. E. M. Toes The Tumoricidal Activity of Memory CD8+ T Cells Is Hampered by Persistent Systemic Antigen, but Full Functional Capacity Is Regained in an Antigen-Free Environment J. Immunol., May 15, 2004; 172(10): 6074 - 6079. [Abstract] [Full Text] [PDF]
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M. L. Salem, A. N. Kadima, Y. Zhou, C. L. Nguyen, M. P. Rubinstein, M. Demcheva, J. N. Vournakis, D. J. Cole, and W. E. Gillanders Paracrine Release of IL-12 Stimulates IFN-{gamma} Production and Dramatically Enhances the Antigen-Specific T Cell Response after Vaccination with a Novel Peptide-Based Cancer Vaccine J. Immunol., May 1, 2004; 172(9): 5159 - 5167. [Abstract] [Full Text] [PDF]
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L. Haynes, S. M. Eaton, E. M. Burns, M. Rincon, and S. L. Swain Inflammatory Cytokines Overcome Age-Related Defects in CD4 T Cell Responses In Vivo J. Immunol., May 1, 2004; 172(9): 5194 - 5199. [Abstract] [Full Text] [PDF]
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D. M. Richards, S. L. Dalheimer, B. D. Ehst, T. L. Vanasek, M. K. Jenkins, M. I. Hertz, and D. L. Mueller Indirect Minor Histocompatibility Antigen Presentation by Allograft Recipient Cells in the Draining Lymph Node Leads to the Activation and Clonal Expansion of CD4+ T Cells That Cause Obliterative Airways Disease J. Immunol., March 15, 2004; 172(6): 3469 - 3479. [Abstract] [Full Text] [PDF]
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J. Chang, J.-H. Cho, S.-W. Lee, S.-Y. Choi, S.-J. Ha, and Y.-C. Sung IL-12 Priming during In Vitro Antigenic Stimulation Changes Properties of CD8 T Cells and Increases Generation of Effector and Memory Cells J. Immunol., March 1, 2004; 172(5): 2818 - 2826. [Abstract] [Full Text] [PDF]
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S. Baize, J. Kaplon, C. Faure, D. Pannetier, M.-C. Georges-Courbot, and V. Deubel Lassa Virus Infection of Human Dendritic Cells and Macrophages Is Productive but Fails to Activate Cells J. Immunol., March 1, 2004; 172(5): 2861 - 2869. [Abstract] [Full Text] [PDF]
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D. Palliser, Q. Huang, N. Hacohen, S. P. Lamontagne, E. Guillen, R. A. Young, and H. N. Eisen A Role for Toll-Like Receptor 4 in Dendritic Cell Activation and Cytolytic CD8+ T Cell Differentiation in Response to a Recombinant Heat Shock Fusion Protein J. Immunol., March 1, 2004; 172(5): 2885 - 2893. [Abstract] [Full Text] [PDF]
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S. Walter, L. Herrgen, O. Schoor, G. Jung, D. Wernet, H.-J. Buhring, H.-G. Rammensee, and S. Stevanovic Cutting Edge: Predetermined Avidity of Human CD8 T Cells Expanded on Calibrated MHC/Anti-CD28-Coated Microspheres J. Immunol., November 15, 2003; 171(10): 4974 - 4978. [Abstract] [Full Text] [PDF]
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J. M. Curtsinger, C. M. Johnson, and M. F. Mescher CD8 T Cell Clonal Expansion and Development of Effector Function Require Prolonged Exposure to Antigen, Costimulation, and Signal 3 Cytokine J. Immunol., November 15, 2003; 171(10): 5165 - 5171. [Abstract] [Full Text] [PDF]
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B. T. Endrizzi and S. C. Jameson Differential role for IL-7 in inducing lung Kruppel-like factor (Kruppel-like factor 2) expression by naive versus activated T cells Int. Immunol., November 1, 2003; 15(11): 1341 - 1348. [Abstract] [Full Text] [PDF]
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J. Liu, C. S. Schmidt, F. Zhao, A. J. Okragly, A. Glasebrook, N. Fox, E. Galbreath, Q. Zhang, H. Y. Song, S. Na, et al. LIGHT-deficiency impairs CD8+ T cell expansion, but not effector function Int. Immunol., July 1, 2003; 15(7): 861 - 870. [Abstract] [Full Text] [PDF]
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A. Dolganiuc, K. Kodys, A. Kopasz, C. Marshall, T. Do, L. Romics Jr., P. Mandrekar, M. Zapp, and G. Szabo Hepatitis C Virus Core and Nonstructural Protein 3 Proteins Induce Pro- and Anti-inflammatory Cytokines and Inhibit Dendritic Cell Differentiation J. Immunol., June 1, 2003; 170(11): 5615 - 5624. [Abstract] [Full Text] [PDF]
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 L. Krishnan, S. Sad, G. B. Patel, and G. D. Sprott Archaeosomes Induce Enhanced Cytotoxic T Lymphocyte Responses to Entrapped Soluble Protein in the Absence of Interleukin 12 and Protect against Tumor Challenge Cancer Res., May 15, 2003; 63(10): 2526 - 2534. [Abstract] [Full Text] [PDF]
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J. M. Curtsinger, D. C. Lins, and M. F. Mescher Signal 3 Determines Tolerance versus Full Activation of Naive CD8 T Cells: Dissociating Proliferation and Development of Effector Function J. Exp. Med., May 5, 2003; 197(9): 1141 - 1151. [Abstract] [Full Text] [PDF]
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 J. E. A. Portielje, C. H. J. Lamers, W. H. J. Kruit, A. Sparreboom, R. L. H. Bolhuis, G. Stoter, C. Huber, and J. W. Gratama Repeated Administrations of Interleukin (IL)-12 Are Associated with Persistently Elevated Plasma Levels of IL-10 and Declining IFN-{gamma}, Tumor Necrosis Factor-{alpha}, IL-6, and IL-8 Responses Clin. Cancer Res., January 1, 2003; 9(1): 76 - 83. [Abstract] [Full Text] [PDF]
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J. Goldberg, P. Shrikant, and M. F. Mescher In Vivo Augmentation of Tumor-Specific CTL Responses by Class I/Peptide Antigen Complexes on Microspheres (Large Multivalent Immunogen) J. Immunol., January 1, 2003; 170(1): 228 - 235. [Abstract] [Full Text] [PDF]
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J. Valenzuela, C. Schmidt, and M. Mescher The Roles of IL-12 in Providing a Third Signal for Clonal Expansion of Naive CD8 T Cells J. Immunol., December 15, 2002; 169(12): 6842 - 6849. [Abstract] [Full Text] [PDF]
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Y.-Z. Wu, J.-P. Zhao, Y. Wan, Z.-C. Jia, W. Zhou, J. Bian, B. Ni, L.-Y. Zou, and Y. Tang Mimovirus: a Novel Form of Vaccine That Induces Hepatitis B Virus-Specific Cytotoxic T-Lymphocyte Responses In Vivo J. Virol., September 11, 2002; 76(20): 10264 - 10269. [Abstract] [Full Text] [PDF]
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 D. J. Naisbitt, J. Farrell, S. F. Gordon, J. L. Maggs, C. Burkhart, W. J. Pichler, M. Pirmohamed, and B. K. Park Covalent Binding of the Nitroso Metabolite of Sulfamethoxazole Leads to Toxicity and Major Histocompatibility Complex-Restricted Antigen Presentation Mol. Pharmacol., September 1, 2002; 62(3): 628 - 637. [Abstract] [Full Text] [PDF]
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J. Hernandez, S. Aung, K. Marquardt, and L. A. Sherman Uncoupling of Proliferative Potential and Gain of Effector Function by CD8+ T Cells Responding to Self-Antigens J. Exp. Med., August 5, 2002; 196(3): 323 - 333. [Abstract] [Full Text] [PDF]
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C. S. Schmidt and M. F. Mescher Peptide Antigen Priming of Naive, But Not Memory, CD8 T Cells Requires a Third Signal That Can Be Provided by IL-12 J. Immunol., June 1, 2002; 168(11): 5521 - 5529. [Abstract] [Full Text] [PDF]
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A. D. Higgins, M. A. Mihalyo, P. W. McGary, and A. J. Adler CD4 Cell Priming and Tolerization Are Differentially Programmed by APCs upon Initial Engagement J. Immunol., June 1, 2002; 168(11): 5573 - 5581. [Abstract] [Full Text] [PDF]
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J. Gong, S. Koido, D. Chen, Y. Tanaka, L. Huang, D. Avigan, K. Anderson, T. Ohno, and D. Kufe Immunization against murine multiple myeloma with fusions of dendritic and plasmacytoma cells is potentiated by interleukin 12 Blood, April 1, 2002; 99(7): 2512 - 2517. [Abstract] [Full Text] [PDF]
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R. Xiang, F. J. Primus, J. M. Ruehlmann, A. G. Niethammer, S. Silletti, H. N. Lode, C. S. Dolman, S. D. Gillies, and R. A. Reisfeld A Dual-Function DNA Vaccine Encoding Carcinoembryonic Antigen and CD40 Ligand Trimer Induces T Cell-Mediated Protective Immunity Against Colon Cancer in Carcinoembryonic Antigen-Transgenic Mice J. Immunol., October 15, 2001; 167(8): 4560 - 4565. [Abstract] [Full Text] [PDF]
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 P. Lee, F. Wang, J. Kuniyoshi, V. Rubio, T. Stuges, S. Groshen, C. Gee, R. Lau, G. Jeffery, K. Margolin, et al. Effects of Interleukin-12 on the Immune Response to a Multipeptide Vaccine for Resected Metastatic Melanoma J. Clin. Oncol., September 15, 2001; 19(18): 3836 - 3847. [Abstract] [Full Text] [PDF]
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A. V. Gorbachev, N. A. DiIulio, and R. L. Fairchild IL-12 Augments CD8+ T Cell Development for Contact Hypersensitivity Responses and Circumvents Anti-CD154 Antibody-Mediated Inhibition J. Immunol., July 1, 2001; 167(1): 156 - 162. [Abstract] [Full Text] [PDF]
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W. C. Kieper, M. Prlic, C. S. Schmidt, M. F. Mescher, and S. C. Jameson IL-12 Enhances CD8 T Cell Homeostatic Expansion J. Immunol., May 1, 2001; 166(9): 5515 - 5521. [Abstract] [Full Text] [PDF]
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S. Koido, M. Kashiwaba, D. Chen, S. Gendler, D. Kufe, and J. Gong Induction of Antitumor Immunity by Vaccination of Dendritic Cells Transfected with MUC1 RNA J. Immunol., November 15, 2000; 165(10): 5713 - 5719. [Abstract] [Full Text] [PDF]
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R. Mortarini, A. Borri, G. Tragni, I. Bersani, C. Vegetti, E. Bajetta, S. Pilotti, V. Cerundolo, and A. Anichini Peripheral Burst of Tumor-specific Cytotoxic T Lymphocytes and Infiltration of Metastatic Lesions by Memory CD8+ T Cells in Melanoma Patients Receiving Interleukin 12 Cancer Res., July 1, 2000; 60(13): 3559 - 3568. [Abstract] [Full Text]
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S. L. Schober, C. T. Kuo, K. S. Schluns, L. Lefrancois, J. M. Leiden, and S. C. Jameson Expression of the Transcription Factor Lung Kruppel-Like Factor Is Regulated by Cytokines and Correlates with Survival of Memory T Cells In Vitro and In Vivo J. Immunol., October 1, 1999; 163(7): 3662 - 3667. [Abstract] [Full Text] [PDF]
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R. Xiang, H. N. Lode, S. D. Gillies, and R. A. Reisfeld T Cell Memory Against Colon Carcinoma Is Long-Lived in the Absence of Antigen J. Immunol., October 1, 1999; 163(7): 3676 - 3683. [Abstract] [Full Text] [PDF]
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C. S. Schmidt and M. F. Mescher Adjuvant Effect of IL-12: Conversion of Peptide Antigen Administration from Tolerizing to Immunizing for CD8+ T Cells In Vivo J. Immunol., September 1, 1999; 163(5): 2561 - 2567. [Abstract] [Full Text] [PDF]
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5 divisions these are: transfer only
88%, 2%, and 9%; peptide only 1%, 72%, and 28%; peptide + IL-12
1%, 32%, and 67%; peptide + CFA 6%, 12%, and 82%. 2C cells in
mice stimulated with peptide only do not exhibit further dilution of
dye beyond day 3 (data not shown). Essentially identical results were
obtained in two independent experiments.