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Production by Dendritic Cells1
Department of Microbiology and Immunology, Keio University School of Medicine, Tokyo, Japan
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Abstract |
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 Top Abstract IntroductionMaterials and MethodsResultsDiscussionReferences |
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in response to
IL-12. In the present study, we analyzed effects of Th1 and Th2
cytokines on IFN- production by DCs. IL-18 produced by DCs and
macrophages acts in an autocrine manner and augments IL-12-induced
IFN- production by DCs as also observed in T and NK cells.
Surprisingly, IL-4, a Th2 cytokine, also acts synergistically with
IL-12 on IFN- production by DCs. In addition, IL-4 markedly enhances
IFN- production when DCs are stimulated through CD40 or MHC class
II. These results indicate that both Th1 and Th2 cytokines act on DCs
during T cell-DC interaction upon Ag presentation. p38
mitogen-activated protein kinase is constitutively activated in mature
DCs and is required for IFN- production by DCs. IL-18 but not IL-4
or IL-12 further activates the p38 mitogen-activated protein kinase
activity, suggesting that IL-4 and IL-18 enhance IFN- production
through distinct intracellular signal transduction pathways in
DCs. |
Introduction |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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IL-12 acts on T and NK cells to induce the production of IFN-.
Cumulative evidence has shown the importance of IFN- in both innate
and acquired immunity (8, 9, 10, 11, 12, 13, 14, 15). It has long been assumed
that the only cells producing IFN- in
response to IL-12 are T and NK cells. However, recent studies have
shown that macrophages and B cells are also capable of producing
IFN- in response to IL-12 (16, 17, 18). Furthermore, we
have demonstrated that DCs are also able to produce significant amounts
of this cytokine upon Listeria monocytogenes infection or
IL-12 administration (19), suggesting the presence of an
autocrine-positive feed back pathway in APCs.
Action of IL-12 is influenced by other cytokines such as IL-18. IL-18,
originally designated as IFN--inducing factor, strongly augments
IFN- production by T cells, cytotoxicity of NK cells, and T cell
proliferation (20). IL-18 acts synergistically with IL-12
in inducing IFN- from T cells undergoing differentiation to Th1
cells as well as committed Th1 cells. IL-18 also induces IFN-
production by NK cells in both mouse and human (20, 21).
Thus, it has been suggested that both IL-12 and IL-18 are required for
effective differentiation of Th1 cells. In contrast to IL-12 and
IFN-, the Th2-type cytokines, IL-4 and IL-10, show inhibitory
effects on IFN- production by T cells (22, 23).
Furthermore, these cytokines are reported to suppress DC functions
(1, 4, 24, 25, 26).
Recent studies on molecular mechanisms regulating IFN- gene
expression in T cells have shown the importance of p38
mitogen-activated protein kinase (MAPK) pathway (27). p38,
a member of the MAPK superfamily, is activated by various stimuli, such
as proinflammatory cytokines (e.g., IL-1ß and TNF-
), LPS, and
various environmental stresses (heat, osmotic stress, UV irradiation)
(28, 29, 30, 31). p38 MAPK has been implicated in the regulation
of expression of many cytokine genes (27, 32, 33, 34).
Because various stimuli are able to activate DCs to secrete IL-12 and
then IFN-, it is of interest to examine the role of other cytokines
and the molecular mechanisms of regulation of IFN- production by
DCs. Here we report synergistic action of IL-4 as well as IL-18 with
IL-12 in augmenting IFN- production by DCs. In contrast, IL-10 has
no effect on the ability of DCs to produce IFN-. We further show
that p38 MAPK activities are important in IFN- production by
DCs.
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Materials and Methods |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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C57BL/6 mice were purchased from Sankyo Labo Service (Tokyo, Japan). B10.D2-recombinase activating gene (Rag)-2-deficient mice, Rag-2-/- mice that had been backcrossed to B10.D2/nSnJ for 10 generations (Ref. 19 and S.K., unpublished observations), were obtained from Taconic (Germantown, NY). All mice were maintained in specific pathogen-free conditions in our animal facility and used between 6 and 12 wk of age. All experiments were performed in accordance with our Institutional Guidelines.
Abs, cytokines, and reagents
The following mAbs were purchased from PharMingen (San Diego,
CA): HL3-FITC, -PE (anti-CD11c); 53-6.7-PE, -biotin
(anti-CD8); PO3-biotin (anti-CD86); purified C17.8
(anti-mIL-12p40/p70); purified 3/23 (anti-CD40). Anti-mouse
I-Ab,k mAb was purchased from Chemicon
International (Temecula, CA). Rabbit polyclonal anti-asialoGM1
(-ASGM1) Ab was purchased from Wako Pure Chemical Industries (Osaka,
Japan). Affinity-purified rabbit anti-p38 MAPK Ab was obtained from
Santa Cruz Biotechnology (Santa Cruz, CA). Recombinant mouse IL-12 was
purchased from Sigma (St. Louis, MO). Recombinant mouse IL-18 and
anti-mouse IL-18 mAb were purchased from MBL (Nagoya, Japan).
Recombinant mouse IL-10 was purchased from Pharma Biotechnologie
Hannover (Hannover, Germany). Purified recombinant mouse IL-4 (100
U/ng) expressed in a baculovirus system (35) was a
generous gift from A. Miyajima (Tokyo University, Tokyo, Japan). A p38
MAPK-specific inhibitor, SB203580, was obtained from Calbiochem (San
Diego, CA). RPMI 1640 supplemented with 10% FCS (HyClone, Logan, UT),
2-ME (50 µM), L-glutamine (2 mM), penicillin (100
U/ml), streptomycin (100 µg/ml), and sodium pyruvate (1 mM) was used
as the complete culture medium (CM).
DC preparation
DCs were prepared from collagenase-digested spleens (Collagenase
D; Boehringer Mannheim, Indianapolis, IN), as described previously
(19, 36). Briefly, collagenase-digested spleen cells were
suspended in a dense BSA solution in PBS (p =
1.080; Sigma), overlaid with 1 ml of FCS-free RPMI 1640 medium, and
centrifuged in a swing bucket rotor at 9500 x g for 20
min at 4°C. The cells in a low-density fraction at the interface were
collected and washed twice. The cells were resuspended in CM and
allowed to adhere to plastic dishes for 2 h. After nonadherent
cells were depleted, adherent cells were incubated for an additional
18 h to allow DCs to detach. After this incubation, floating cells
were collected and DCs were positively purified using anti-CD11c
(N418) MicroBeads and a magnetic cell separation system column
(Miltenyi Biotec, Bergisch Gladbach, Germany). Purified cells were
routinely >94% CD11c+
I-A+. In some experiments, the nonadherent cell
fraction from the overnight incubation procedure was stained with a
mixture of the following biotinylated mAbs: anti-CD3
, 145-2C11;
anti-CD4, GK1.5; anti-B220, RA3-6B2. Cells were then incubated
with streptavidin MicroBeads and depleted by magnetic cell separation
system (Miltenyi Biotec). After this depletion, purity of DCs was
>80%. An additional purification procedure was done to separate DCs
into CD8+ and CD8-
subsets. The CD8+ subset was positively
selected with anti-CD8 (Ly-2) MicroBeads (Miltenyi Biotec), and,
from the negative fraction of this selection, the
CD8- subset was purified with anti-CD11c
(N418) MicroBeads (Miltenyi Biotec).
Flow cytometric analysis
Cells were stained with FITC-, PE-, or biotin-conjugated mAbs in PBS-2% FCS, washed, and analyzed on a FACScan using the CELLQuest program (Becton Dickinson, San Jose, CA). Biotinylated mAbs were detected with streptavidin Red 670 (Life Technologies, Gaithersburg, MD).
p38 kinase assay
Purified DCs (2 x 106 in 1 ml CM)
were stimulated with cytokines for indicated time periods and lysed in
a lysis buffer solution consisting of 20 mM Tris-HCl, pH 7.4, 12.5 mM
ß-glycerophosphate, 2 mM EGTA, 10 mM NaF, 1 mM benzamidine, 1%
Triton X-100, 2 mM DTT, 1 mM sodium orthovanadate, 1% aprotinin, 1 mM
PMSF, 10 µg/ml leupeptin, and 10 µg/ml pepstatin A. The lysates
were centrifuged at 15,000 x g for 30 min, and p38
MAPK was immunoprecipitated from the postnuclear supernatant with
anti-p38 Ab and protein A-Sepharose beads (Amersham, Arlington
Heights, IL). The precipitates were washed twice with a buffer solution
consisting of 20 mM Tris-HCl, pH 7.5, 500 mM NaCl, 0.05% Tween 20, and
once with an extraction buffer solution consisting of 20 mM Tris-HCl,
pH 7.4, 12.5 mM ß-glycerophosphate, 2 mM EGTA, 10 mM NaF, 1 mM
benzamidine, and 2 mM DTT. Samples were then mixed with 3 µg of
His-tagged ATF2 in the presence of 50 µM ATP, 10 mM
MgCl2, and 74 kBq of
[-32P]ATP and incubated at 30°C for 20 min
in a final volume of 15 µl. Reactions were terminated by boiling in a
Laemmli’s sample buffer solution, resolved by SDS-PAGE, and
radioactivities were quantified on an image analyzer, BAS2000 (Fujix,
Tokyo, Japan).
Cytokine assays
Titers of IFN- in the culture supernatants were determined by
Quantikine M ELISA kit (R&D Systems, Minneapolis, MN), mouse IFN-
ELISA kit (Endogen, Woburn, MA), or mouse IFN- ELISA kit,
Intertest- (Genzyme, Cambridge, MA). It was noted that the titers
obtained by Genzyme kits were always one-fifth of those obtained by the
other two ELISA kits. Therefore, when Genzyme kits were used in an
experiment, it is stated in the figure legend.
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Results |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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production
As shown previously (19), mouse splenic DCs produce
high levels of IFN- in response to IL-12 stimulation (Fig. 1
, A and B).
Because IL-18 strongly augments IFN- production by T, B, and NK
cells, we examined the effect of IL-18 on IFN- production by DCs.
Purified DCs were cultured for 3 days in the presence of IL-12 with
various concentrations of IL-18, and the amounts of IFN- in the
culture supernatants were determined by ELISA. As shown in Fig. 1C, we found that IL-18 dramatically enhances
IL-12-dependent IFN- production by DCs in a dose-dependent manner.
However, IL-18 alone had little effect on IFN- production without
IL-12. The same results were obtained with DCs isolated from -ASGM1
Ab-treated Rag-2-/- mice (19),
indicating that the effect of IL-18 is not due to contaminated
lymphocytes (Fig. 1D). These results indicate that IL-18
acts on DCs synergistically with IL-12 to produce IFN- in a way
similar to its action on T, B, and NK cells and macrophages (17, 18, 20).
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production by DCs
Th2-type cytokines, IL-4 and IL-10, are known to suppress IFN-
production by T cells (22, 23). Thus, we investigated
whether IL-4 and IL-10 also suppress IFN- production by DCs. To our
surprise, IL-4 dramatically augmented IL-12-induced IFN- production
by DCs in a dose-dependent manner, whereas IL-4 alone had no effect
(Fig. 2A). These results
indicate that IL-4 also acts synergistically with IL-12 on IFN-
production by DCs. Although not shown, IL-4 from four different sources
were used with consistent results. In contrast to IL-4, IL-10 showed no
significant effect. IL-10 neither enhanced nor inhibited IFN-
production by DCs (Fig. 2B). Furthermore, IL-10 showed no
effect on the synergistic effect of IL-4 (Fig. 2C). Action
of IL-4 does not involve IL-18 produced by DCs because addition of
anti-IL-18 mAb had no effect on IL-4 action (Fig. 2C).
These results collectively show that a Th2 cytokine, IL-4, acts
synergistically with IL-12 on IFN- production by DCs, whereas IL-10,
another Th2 cytokine, has no effect.
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production by DCs
DCs produce IL-12 upon various stimuli through different
mechanisms such as microbial invasion and T cell-DC interaction
(2, 3, 4, 5, 37). The latter is dependent on CD40-CD40L (CD154)
and/or MHC class II-TCR interaction (3, 4, 5). Thus, it is
possible that endogenous IL-12 production resulting from CD40-CD40L
interaction or MHC class II-TCR ligation induces IFN- production by
DCs. To this end, purified DCs were cultured in the presence of
anti-CD40 or anti-MHC class II mAbs, and IFN- production was
examined by ELISA. As expected, both CD40 cross-linking by
anti-CD40 mAb and MHC class II cross-linking by anti-MHC class
II mAb induced IFN- production by DCs (Fig. 3, A and B).
Addition of neutralizing mAb against IL-12 markedly suppressed IFN-
production by CD40 or MHC class II cross-linking. Thus, IFN-
production by CD40 or MHC class II cross-linking is likely
dependent on endogenous IL-12 in an autocrine manner. IL-4 was also
shown to synergistically induce IFN- production by anti-CD40 mAb
and anti-MHC class II mAb (Fig. 3, C and D).
Anti-IL-12 mAb blocked such synergistic effect of IL-4, indicating that
IL-4 also favors IL-12-dependent IFN- production during DC-T cell
interaction.
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myeloid as well as CD8+ lymphoid DCs in IFN-
production
In the mouse, two distinct DC populations are present in the
spleen.
CD8+DEC205+CD11b-
and
CD8-DEC205-CD11b+
DC represent lymphoid and myeloid DCs, respectively (38).
It has been reported that they differ in their ability to induce
Th1/Th2 responses (2, 7, 39, 40). Furthermore, we have
previously demonstrated that CD8+ DCs are the
major IFN- producers in response to IL-12 stimulation
(19). These results prompted us to compare how IL-4 and
IL-18 act on these subsets for IFN- production.
CD8+ and CD8- DCs
were isolated (Fig. 4A) and
cultured for 3 days in the presence of IL-12 alone or in combination
with IL-4 or IL-18. When cultured with IL-12 alone,
CD8+ DCs produced significantly higher levels
of IFN- than CD8- DCs did (the ratio of
amounts produced was about 5:1) as shown previously (19).
Interestingly, when IL-4 or IL-18 are present with IL-12, no difference
was observed between two DC subsets in the amounts of IFN-
production (Fig. 4B). The CD8- DC
subset is thus capable of producing high amounts of IFN- in the
presence of IL-4 or IL-18 together with IL-12.
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production by DCs and
augmented by IL-18 but not by IL-4
A MAPK superfamily member, p38 MAPK, is implicated in regulating
the expression of various cytokine genes (27, 32, 33, 34). It
has recently been reported that p38 MAPK is required for IFN-
production in Th1 cells (27). Thus, we examined whether
p38 MAPK is involved in the IFN- production by DCs. Purified DCs
were stimulated with IL-12 alone or in combination with IL-4 or IL-18,
and p38 MAPK activities were measured. As shown in Fig. 5A, activity of p38 MAPK was
readily detected in nonstimulated DCs, and IL-12 did not increase the
p38 MAPK activity. When DCs were stimulated with a combination of IL-12
and IL-18, a 2-fold increase in p38 MAPK activity was observed. In
contrast, IL-4 had no effect on p38 MAPK activity. These results imply
that p38 MAPK is constitutively activated in mature DCs at a low level,
and IL-18 but not IL-12 or IL-4 augments its activity.
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by DCs. As shown in Fig. 5
B, a,
SB203580 inhibited IFN- production in a dose-dependent manner when
DCs were stimulated with IL-12. Similarly, SB203580 inhibits IFN-
production by DCs stimulated by IL-12 in combination with IL-4 or IL-18
(Fig. 5B, b and c). The presence of SB203580 did
not affect the viability of the cells when culture supernatants were
harvested (data not shown). From these results, we conclude that the
basal activity of p38 MAPK in mature DCs is required for IL-12-induced
IFN- production. |
Discussion |
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TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
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-inducing factor (20, 21), which with IL-12 synergistically activates IFN-
production in T, B, and NK cells (17, 42, 43, 44). We show
here that IL-18 also acts synergistically with IL-12 for IFN-
production by DCs. In T and B cells, up-regulation of IL-18 receptor
expression by IL-12 stimulation is one prevailing explanation for the
synergism of IL-12 and IL-18 on IFN- induction (44, 45). Mature DCs constitutively produce small amounts of IL-12
and anti-IL-12 mAb completely blocks basal level of IFN-
production by DCs (Fig. 1B). We found that DCs express IL-18
receptor mRNA as detected by RT-PCR without exogenous IL-12 stimulation
(our unpublished observation). It is possible that endogenous IL-12
production results in the expression of IL-18 receptors on DCs. Thus
activation of DCs by phagocytosis or microbial infection likely leads
to the production of higher amounts of IL-12, which further up-regulate
IL-18 receptor expression.
As shown here, DCs can produce IFN- in response to IL-12 and IL-18,
both of which are produced by DCs (46). These results
suggest a novel role of DCs in innate and acquired immunity. The
importance of rapid IFN- production has been shown in innate
immunity such as in the immediate response to L.
monocytogenes and T. gondii infection (2, 8, 11, 13, 19). Based on our results and recent reports, we propose a
model of acute IFN- production in the innate immune response (Fig. 6A). In response to pathogens
such as T. gondii, IL-12 is produced by DCs independently
from T cells (2) and triggers an IL-12 autocrine pathway
and IFN- production by DCs (19, 37). IFN-
subsequently activates macrophages to produce IL-12 and IL-18
(20, 47, 48), both of which act on DCs and macrophages to
further induce IFN- production (18). Such a positive
feedback cycle results in amplification of IFN- in the innate immune
response. As demonstrated here, IL-18 also acts on DCs and macrophages
in an autocrine manner for IFN- production. In addition, IFN-
derived from DCs likely influences Th1 induction in acquired immunity
by acting on T cells during Ag presentation (9, 10).
Recent reports provide strong evidence for the importance of DCs in
driving Th1 and Th2 responses (7, 39, 40, 49). IL-18
presumably acts on Th1 induction as a potent enhancer of IFN-
production by DCs.
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production by DCs. IFN- and IL-4 are typical cytokines
produced by Th1 and Th2 cells, respectively, and suppress the
differentiation of Th2 and Th1, respectively (15, 50). Our
findings clearly contradict the general view that IL-4 suppresses
IFN- production. However, it should be noted that several groups
have previously observed phenomena that are consistent with our
findings. First, experimental autoimmune uveoretinitis is a typical
Th1-dependent disease. In contrast to the expectation, IL-4-treated
rats in an experimental autoimmune uveoretinitis model showed an
aggravation of symptoms, and the amounts of IFN- production were
actually augmented by IL-4 treatment (51). Such enhanced
production of IFN- could be due to either direct activation of DCs
by IL-4 or Th1 activation by DCs exposed to IL-4. Second, in an
Ag-induced arthritis model in mice, treatment with neutralizing
anti-IL-4 mAb inhibited the disease, suggesting that IL-4 plays a
proinflammatory role and can act as a mediator of Th1 development in
this system (52). Third, in addition, it has recently been
reported that IL-4 is required for the development of a Th1 response to
Candida albicans (53); the IFN- production
by CD4+ Th cells was reduced in IL-4-deficient
mice in response to a virulent strain of C. albicans. Based
on our results, it is likely that IL-4 acts on DCs during Ag
presentation and induces IFN- production followed by efficient Th1
induction in these cases.
Lingnau et al. (54) demonstrated a novel alternative
pathway of Th1 induction. IL-4 in combination with TGF-ß favors Th1
development, and this process requires IFN- (54). Our
findings that IL-4 up-regulates IFN- production by DCs strongly
support this novel Th1-inducing pathway. The role of DCs in such a Th1
induction pathway is not only as APCs but also the source of IFN- in
the presence of IL-4. We also showed that IL-4 enhances IFN-
production by DCs upon CD40 or MHC class II cross-linking, which mimics
DC-T cell interaction (Figs. 3 and 6B). In this pathway,
endogenous IL-12 production by DCs seems essential because addition of
anti-IL-12 mAb blocked IFN- production to near basal levels.
Because IFN- is indispensable for the alternative pathway, DCs are
the most likely candidates as the source of IFN- in this
pathway.
It has been shown that DCs can be divided into distinct subsets and
that different subsets of DCs induce different Th subsets (7, 39, 40, 49). In mice, it has been reported that
CD8+ lymphoid DCs induce the Th1-type
response, whereas CD8- myeloid DCs trigger
the Th2-type response in vivo (7, 39, 40). We have
previously demonstrated that IL-12 induces IFN- production
predominantly by CD8+ lymphoid DCs rather than
CD8- myeloid DCs (19), which is
consistent with the notion that CD8+ lymphoid
DCs play a critical role in Th1 induction. We found in the present
study that CD8- myeloid DCs are also capable
of producing high amounts of IFN- when IL-4 or IL-18 coexists with
IL-12, suggesting that both DC subsets produce IFN- when infected
with microorganisms and induced to produce IL-18. In studies reporting
that the distinct DC subsets differed in their capacity to induce Th
subsets, CD8+ and
CD8- DCs were separately isolated in vitro
and reconstituted to in vivo after Ag-pulse (7, 39, 40).
Although it is likely that CD8+ lymphoid DCs
and CD8- myeloid DCs have intrinsic
characteristics for induction of Th1 and Th2 responses, respectively,
pathogens are likely presented to T cells by both DC subsets in actual
infection. Various other factors involved in Ag presentation by DCs
during induction of Th subsets must be investigated to understand the
molecular mechanisms of Th1/Th2 differentiation.
In this study, the role of p38 MAPK in IFN- production by DCs was
also investigated. Involvement of p38 MAPK has been implicated in
IFN- production by Th1 cells (27). We found that the
specific inhibitor of p38 MAPK, SB203580, suppresses IFN- production
by DCs in response to IL-12 alone or in combination with IL-4 or IL-18,
suggesting the importance of p38 MAPK in IFN- production by DCs. p38
MAPK activity is readily observed in isolated DCs and is not enhanced
by IL-12 (Fig. 5). Rescigno et al. (55) reported that MAPK
family members c-Jun N-terminal kinase, p38, and extracellular
signal-regulated kinase were activated during LPS-induced
maturation of an immortalized immature mouse splenic DC line. Because
DCs present in the spleen are in an immature stage and induced to
maturate during isolation procedures by unknown mechanisms (1, 56), it is likely that p38 MAPK is already activated and its
activity is maintained in mature DCs. The fact that p38 MAPK activity
is unaltered by IL-12 yet SB203580 inhibits IL-12-induced IFN-
production indicates that the basal activity of p38 MAPK in mature DCs
is required for the IL-12 signaling. Although IL-4 and IL-18
synergistically induced IFN- production, only IL-18 augments p38
MAPK activity. This finding suggests that the increase in p38 MAPK
activity is one of the mechanisms of the synergistic effect of IL-18
for IL-12-induced IFN- production by DCs. The mechanism of
synergistic effect of IL-4 is different from that of IL-18 and remains
to be examined. Because IL-4 acts on both mouse and human bone marrow-
or monocyte-derived DCs induced by GM-CSF (57, 58), it is
possible that IL-4 modulates some maturation or growth state of DCs
during culture, influencing the capacity of DCs to respond to
IL-12.
In summary, we demonstrate synergistic effects of both Th1- and
Th2-type cytokines, namely IL-4 and IL-18, with IL-12 on IFN-
production by DCs. We also demonstrate a role for p38 MAPK pathways in
IL-12-induced IFN- production by DCs. Biochemical analyses show that
IL-4 and IL-18 enhance the effects of IL-12 through distinct
intracellular signaling pathways. Such synergistic effects of IL-4 and
IL-18 are of interest in understanding the role of DCs in both innate
and acquired immunity, especially in the Th1 vs Th2 balance.
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Acknowledgments |
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Footnotes |
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2 Address correspondence and reprint requests to Dr. Shigeo Koyasu, Department of Microbiology and Immunology, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan. E-mail address:
3 Abbreviations used in the paper: DC, dendritic cell; CM, culture medium; MAPK, mitogen-activated protein kinase; Rag, recombinase activation gene; CD40L, CD40 ligand.
Received for publication August 19, 1999. Accepted for publication October 13, 1999.
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References |
|---|
|
TopAbstractIntroductionMaterials and MethodsResultsDiscussionReferences |
|---|
ve CD4+ T cells. J. Immunol. 154:5071.[Abstract]
+ and CD8- subclasses of dendritic cells direct the development of distinct T helper cells in vivo. J. Exp. Med. 189:587. production for resolution of Listeria monocytogenes infection. Proc. Natl. Acad. Sci. USA 82:7404. antibodies in vivo abrogates natural resistance of C3H/HeN mice to infection with Leishmania major. J. Immunol. 143:266.[Abstract]
. Immunity 3:109.[Medline]
production and type 1 cytokine responses. Immunity 4:471.[Medline]
receptor-deficient mice. J. Immunol. 158:5297.[Abstract]
production and innate immunity during Listeria monocytogenes infection in the absence of NK cells. J. Immunol. 161:5600. expression and secretion in mouse peritoneal macrophages. J. Immunol. 159:3490.[Abstract]
production from activated B cells. Proc. Natl. Acad. Sci. USA 94:3948. upon combined stimulation with interleukin (IL)-12 and IL-18: a novel pathway of autocrine macrophage activation. J. Exp. Med. 187:2103. production by CD8+ lymphoid dendritic cells. J. Exp. Med. 189:1981. production by T cells. Nature 378:88.[Medline]
inducing factor, expression in Escherichia coli, and studies on the biological activities of the protein. J. Immunol. 156:4274.[Abstract]
expression by Th1 effector T cells mediated by the p38 MAP kinase signaling pathway. EMBO J. 17:2817.[Medline]
B and primes DC for IL-12 production. Immunity 9:315.[Medline]
+ dendritic cells generate an immune response after subcutaneous injection without homing to the draining lymph node. J. Exp. Med. 189:593. production and activates IRAK and NFB. Immunity 7:571.[Medline]
production. J. Immunol. 161:3400. -inducing factor and regulates LPS-induced IFN- production. Nature 386:619.[Medline]
inducing factor mediated by interleukin-1ß converting enzyme. Science 275:206.. J. Exp. Med. 179:1109.This article has been cited by other articles:
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T. Tomizawa, Y. Kaneko, Y. Kaneko, Y. Saito, H. Ohnishi, J. Okajo, C. Okuzawa, T. Ishikawa-Sekigami, Y. Murata, H. Okazawa, et al. Resistance to Experimental Autoimmune Encephalomyelitis and Impaired T Cell Priming by Dendritic Cells in Src Homology 2 Domain-Containing Protein Tyrosine Phosphatase Substrate-1 Mutant Mice J. Immunol., July 15, 2007; 179(2): 869 - 877. [Abstract] [Full Text] [PDF]
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 K. Obayashi, T. Doi, and S. Koyasu Dendritic cells suppress IgE production in B cells Int. Immunol., February 1, 2007; 19(2): 217 - 226. [Abstract] [Full Text] [PDF]
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 U. I. Chaudhry, T. P. Kingham, G. Plitas, S. C. Katz, J. R. Raab, and R. P. DeMatteo Combined Stimulation with Interleukin-18 and CpG Induces Murine Natural Killer Dendritic Cells to Produce IFN-{gamma} and Inhibit Tumor Growth Cancer Res., November 1, 2006; 66(21): 10497 - 10504. [Abstract] [Full Text] [PDF]
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H. Li, W. Wojciechowski, C. Dell'Agnola, N. E. Lopez, and I. Espinoza-Delgado IFN-{gamma} and T-bet Expression in Human Dendritic Cells from Normal Donors and Cancer Patients Is Controlled through Mechanisms Involving ERK-1/2-Dependent and IL-12-Independent Pathways J. Immunol., September 15, 2006; 177(6): 3554 - 3563. [Abstract] [Full Text] [PDF]
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H. Ito, E. Esashi, T. Akiyama, J.-i. Inoue, and A. Miyajima IL-18 produced by thymic epithelial cells induces development of dendritic cells with CD11b in the fetal thymus Int. Immunol., August 1, 2006; 18(8): 1253 - 1263. [Abstract] [Full Text] [PDF]
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 U. I. Chaudhry, S. C. Katz, T. P. Kingham, V. G. Pillarisetty, J. R. Raab, A. B. Shah, and R. P. DeMatteo In vivo overexpression of Flt3 ligand expands and activates murine spleen natural killer dendritic cells FASEB J, May 1, 2006; 20(7): 982 - 984. [Abstract] [Full Text] [PDF]
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I. Fricke, D. Mitchell, J. Mittelstadt, N. Lehan, H. Heine, T. Goldmann, A. Bohle, and S. Brandau Mycobacteria Induce IFN-{gamma} Production in Human Dendritic Cells via Triggering of TLR2 J. Immunol., May 1, 2006; 176(9): 5173 - 5182. [Abstract] [Full Text] [PDF]
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H. Iinuma, K. Okinaga, R. Fukushima, T. Inaba, K. Iwasaki, A. Okinaga, I. Takahashi, and M. Kaneko Superior Protective and Therapeutic Effects of IL-12 and IL-18 Gene-Transduced Dendritic Neuroblastoma Fusion Cells on Liver Metastasis of Murine Neuroblastoma J. Immunol., March 15, 2006; 176(6): 3461 - 3469. [Abstract] [Full Text] [PDF]
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S. Otsu, K. Gotoh, T. Yamashiro, J. Yamagata, K. Shin, T. Fujioka, and A. Nishizono Transfer of Antigen-Pulsed Dendritic Cells Induces Specific T-Cell Proliferation and a Therapeutic Effect against Long-Term Helicobacter pylori Infection in Mice Infect. Immun., February 1, 2006; 74(2): 984 - 993. [Abstract] [Full Text] [PDF]
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A. Suto, H. Nakajima, N. Tokumasa, H. Takatori, S.-i. Kagami, K. Suzuki, and I. Iwamoto Murine Plasmacytoid Dendritic Cells Produce IFN-{gamma} upon IL-4 Stimulation J. Immunol., November 1, 2005; 175(9): 5681 - 5689. [Abstract] [Full Text] [PDF]
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 Y. Sasaki, T. Yoshimoto, H. Maruyama, T. Tegoshi, N. Ohta, N. Arizono, and K. Nakanishi IL-18 with IL-2 protects against Strongyloides venezuelensis infection by activating mucosal mast cell-dependent type 2 innate immunity J. Exp. Med., September 6, 2005; 202(5): 607 - 616. [Abstract] [Full Text] [PDF]
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 S. Tanaka, M. Sato, T. Onitsuka, H. Kamata, and Y. Yokomizo Inflammatory Cytokine Gene Expression in Different Types of Granulomatous Lesions during Asymptomatic Stages of Bovine Paratuberculosis Vet. Pathol., September 1, 2005; 42(5): 579 - 588. [Abstract] [Full Text] [PDF]
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J. S. Bezbradica, A. K. Stanic, N. Matsuki, H. Bour-Jordan, J. A. Bluestone, J. W. Thomas, D. Unutmaz, L. Van Kaer, and S. Joyce Distinct Roles of Dendritic Cells and B Cells in Va14Ja18 Natural T Cell Activation In Vivo J. Immunol., April 15, 2005; 174(8): 4696 - 4705. [Abstract] [Full Text] [PDF]
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C. H. Yun, A. Lundgren, J. Azem, A. Sjoling, J. Holmgren, A.-M. Svennerholm, and B. S. Lundin Natural Killer Cells and Helicobacter pylori Infection: Bacterial Antigens and Interleukin-12 Act Synergistically To Induce Gamma Interferon Production Infect. Immun., March 1, 2005; 73(3): 1482 - 1490. [Abstract] [Full Text] [PDF]
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V. G. Pillarisetty, S. C. Katz, J. I. Bleier, A. B. Shah, and R. P. DeMatteo Natural Killer Dendritic Cells Have Both Antigen Presenting and Lytic Function and in Response to CpG Produce IFN-{gamma} via Autocrine IL-12 J. Immunol., March 1, 2005; 174(5): 2612 - 2618. [Abstract] [Full Text] [PDF]
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L. A. Lyakh, M. Sanford, S. Chekol, H. A. Young, and A. B. Roberts TGF-{beta} and Vitamin D3 Utilize Distinct Pathways to Suppress IL-12 Production and Modulate Rapid Differentiation of Human Monocytes into CD83+ Dendritic Cells J. Immunol., February 15, 2005; 174(4): 2061 - 2070. [Abstract] [Full Text] [PDF]
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 U. Schleicher, A. Hesse, and C. Bogdan Minute numbers of contaminant CD8+ T cells or CD11b+CD11c+ NK cells are the source of IFN-{gamma} in IL-12/IL-18-stimulated mouse macrophage populations Blood, February 1, 2005; 105(3): 1319 - 1328. [Abstract] [Full Text] [PDF]
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A. Mavropoulos, G. Sully, A. P. Cope, and A. R. Clark Stabilization of IFN-{gamma} mRNA by MAPK p38 in IL-12- and IL-18-stimulated human NK cells Blood, January 1, 2005; 105(1): 282 - 288. [Abstract] [Full Text] [PDF]
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A. L. Leisewitz, K. A. Rockett, B. Gumede, M. Jones, B. Urban, and D. P. Kwiatkowski Response of the Splenic Dendritic Cell Population to Malaria Infection Infect. Immun., July 1, 2004; 72(7): 4233 - 4239. [Abstract] [Full Text] [PDF]
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A. G. Rothfuchs, M. R. Kreuger, H. Wigzell, and M. E. Rottenberg Macrophages, CD4+ or CD8+ Cells Are Each Sufficient for Protection against Chlamydia pneumoniae Infection through their Ability to Secrete IFN-{gamma} J. Immunol., February 15, 2004; 172(4): 2407 - 2415. [Abstract] [Full Text] [PDF]
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N. M. Tsuji, H. Tsutsui, E. Seki, K. Kuida, H. Okamura, K. Nakanishi, and R. A. Flavell Roles of caspase-1 in Listeria infection in mice Int. Immunol., February 1, 2004; 16(2): 335 - 343. [Abstract] [Full Text] [PDF]
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 K. Schroder, P. J. Hertzog, T. Ravasi, and D. A. Hume Interferon-{gamma}: an overview of signals, mechanisms and functions J. Leukoc. Biol., February 1, 2004; 75(2): 163 - 189. [Abstract] [Full Text] [PDF]
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P.-H. Chiang, L. Wang, C. A. Bonham, X. Liang, J. J. Fung, L. Lu, and S. Qian Mechanistic Insights into Impaired Dendritic Cell Function by Rapamycin: Inhibition of Jak2/Stat4 Signaling Pathway J. Immunol., February 1, 2004; 172(3): 1355 - 1363. [Abstract] [Full Text] [PDF]
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 R. Blackstock and J. W. Murphy Role of Interleukin-4 in Resistance to Cryptococcus neoformans Infection Am. J. Respir. Cell Mol. Biol., January 1, 2004; 30(1): 109 - 117. [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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M. Jefford, M. Schnurr, T. Toy, K.-A. Masterman, A. Shin, T. Beecroft, T. Y. Tai, K. Shortman, M. Shackleton, I. D. Davis, et al. Functional comparison of DCs generated in vivo with Flt3 ligand or in vitro from blood monocytes: differential regulation of function by specific classes of physiologic stimuli Blood, September 1, 2003; 102(5): 1753 - 1763. [Abstract] [Full Text] [PDF]
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 M. M. Gherardi, J. C. Ramirez, and M. Esteban IL-12 and IL-18 act in synergy to clear vaccinia virus infection: involvement of innate and adaptive components of the immune system J. Gen. Virol., August 1, 2003; 84(8): 1961 - 1972. [Abstract] [Full Text] [PDF]
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J. H. Bream, R. E. Curiel, C.-R. Yu, C. E. Egwuagu, M. J. Grusby, T. M. Aune, and H. A. Young IL-4 synergistically enhances both IL-2- and IL-12-induced IFN-{gamma} expression in murine NK cells Blood, July 1, 2003; 102(1): 207 - 214. [Abstract] [Full Text] [PDF]
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 G. Lugo-Villarino, R. Maldonado-Lopez, R. Possemato, C. Penaranda, and L. H. Glimcher T-bet is required for optimal production of IFN-{gamma} and antigen-specific T cell activation by dendritic cells PNAS, June 24, 2003; 100(13): 7749 - 7754. [Abstract] [Full Text] [PDF]
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A. Ito, A. Matejuk, C. Hopke, H. Drought, J. Dwyer, A. Zamora, S. Subramanian, A. A. Vandenbark, and H. Offner Transfer of Severe Experimental Autoimmune Encephalomyelitis by IL-12- and IL-18-Potentiated T Cells Is Estrogen Sensitive J. Immunol., May 1, 2003; 170(9): 4802 - 4809. [Abstract] [Full Text] [PDF]
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T. Yoshimoto, B. Min, T. Sugimoto, N. Hayashi, Y. Ishikawa, Y. Sasaki, H. Hata, K. Takeda, K. Okumura, L. Van Kaer, et al. Nonredundant Roles for CD1d-restricted Natural Killer T Cells and Conventional CD4+ T Cells in the Induction of Immunoglobulin E Antibodies in Response to Interleukin 18 Treatment of Mice J. Exp. Med., April 21, 2003; 197(8): 997 - 1005. [Abstract] [Full Text] [PDF]
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J. A. Gracie, S. E. Robertson, and I. B. McInnes Interleukin-18 J. Leukoc. Biol., February 1, 2003; 73(2): 213 - 224. [Abstract] [Full Text] [PDF]
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H. Sashinami, A. Nakane, Y. Iwakura, and M. Sasaki Effective Induction of Acquired Resistance to Listeria monocytogenes by Immunizing Mice with In Vivo-Infected Dendritic Cells Infect. Immun., January 1, 2003; 71(1): 117 - 125. [Abstract] [Full Text] [PDF]
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S. Al-Darmaki, H. A. Schenkein, J. G. Tew, and S. E. Barbour Differential Expression of Platelet-Activating Factor Acetylhydrolase in Macrophages and Monocyte-Derived Dendritic Cells J. Immunol., January 1, 2003; 170(1): 167 - 173. [Abstract] [Full Text] [PDF]
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H. Kitaura, N. Nagata, Y. Fujimura, H. Hotokezaka, N. Yoshida, and K. Nakayama Effect of IL-12 on TNF-{alpha}-Mediated Osteoclast Formation in Bone Marrow Cells: Apoptosis Mediated by Fas/Fas Ligand Interaction J. Immunol., November 1, 2002; 169(9): 4732 - 4738. [Abstract] [Full Text] [PDF]
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E. Seki, H. Tsutsui, N. M. Tsuji, N. Hayashi, K. Adachi, H. Nakano, S. Futatsugi-Yumikura, O. Takeuchi, K. Hoshino, S. Akira, et al. Critical Roles of Myeloid Differentiation Factor 88-Dependent Proinflammatory Cytokine Release in Early Phase Clearance of Listeria monocytogenes in Mice J. Immunol., October 1, 2002; 169(7): 3863 - 3868. [Abstract] [Full Text] [PDF]
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N. Shirasugi, A. B. Adams, M. M. Durham, A. E. Lukacher, H. Xu, P. Rees, S. R. Cowan, M. A. Williams, T. C. Pearson, and C. P. Larsen Prevention of Chronic Rejection in Murine Cardiac Allografts: A Comparison of Chimerism- and Nonchimerism-Inducing Costimulation Blockade-Based Tolerance Induction Regimens J. Immunol., September 1, 2002; 169(5): 2677 - 2684. [Abstract] [Full Text] [PDF]
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S. E. Barbour, Y. Ishihara, M. Fakher, S. Al-Darmaki, T. H. Caven, C. P. Shelburne, A. M. Best, H. A. Schenkein, and J. G. Tew Monocyte Differentiation in Localized Juvenile Periodontitis Is Skewed toward the Dendritic Cell Phenotype Infect. Immun., June 1, 2002; 70(6): 2780 - 2786. [Abstract] [Full Text] [PDF]
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R. Maldonado-Lopez, C. Maliszewski, J. Urbain, and M. Moser Cytokines Regulate the Capacity of CD8{alpha}+ and CD8{alpha}- Dendritic Cells to Prime Th1/Th2 Cells In Vivo J. Immunol., October 15, 2001; 167(8): 4345 - 4350. [Abstract] [Full Text] [PDF]
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A. Puig-Kroger, M. Relloso, O. Fernandez-Capetillo, A. Zubiaga, A. Silva, C. Bernabeu, and A. L. Corbi Extracellular signal-regulated protein kinase signaling pathway negatively regulates the phenotypic and functional maturation of monocyte-derived human dendritic cells Blood, October 1, 2001; 98(7): 2175 - 2182. [Abstract] [Full Text] [PDF]
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A. E. Morelli, A. F. Zahorchak, A. T. Larregina, B. L. Colvin, A. J. Logar, T. Takayama, L. D. Falo, and A. W. Thomson Cytokine production by mouse myeloid dendritic cells in relation to differentiation and terminal maturation induced by lipopolysaccharide or CD40 ligation Blood, September 1, 2001; 98(5): 1512 - 1523. [Abstract] [Full Text] [PDF]
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Z. Trobonjaca, F. Leithauser, P. Moller, R. Schirmbeck, and J. Reimann Activating Immunity in the Liver. I. Liver Dendritic Cells (but Not Hepatocytes) Are Potent Activators of IFN-{gamma} Release by Liver NKT Cells J. Immunol., August 1, 2001; 167(3): 1413 - 1422. [Abstract] [Full Text] [PDF]
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D. Stober, R. Schirmbeck, and J. Reimann IL-12/IL-18-Dependent IFN-{{gamma}} Release by Murine Dendritic Cells J. Immunol., July 15, 2001; 167(2): 957 - 965. [Abstract] [Full Text] [PDF]
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H. Kang and Y. Suzuki Requirement of Non-T Cells That Produce Gamma Interferon for Prevention of Reactivation of Toxoplasma gondii Infection in the Brain Infect. Immun., May 1, 2001; 69(5): 2920 - 2927. [Abstract] [Full Text] [PDF]
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H. Hochrein, K. Shortman, D. Vremec, B. Scott, P. Hertzog, and M. O'Keeffe Differential Production of IL-12, IFN-{{alpha}}, and IFN-{{gamma}} by Mouse Dendritic Cell Subsets J. Immunol., May 1, 2001; 166(9): 5448 - 5455. [Abstract] [Full Text] [PDF]
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N. J. Horwood, J. Elliott, T. J. Martin, and M. T. Gillespie IL-12 Alone and in Synergy with IL-18 Inhibits Osteoclast Formation In Vitro J. Immunol., April 15, 2001; 166(8): 4915 - 4921. [Abstract] [Full Text] [PDF]
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T. Fukao, D. M. Frucht, G. Yap, M. Gadina, J. J. O'Shea, and S. Koyasu Inducible Expression of Stat4 in Dendritic Cells and Macrophages and Its Critical Role in Innate and Adaptive Immune Responses J. Immunol., April 1, 2001; 166(7): 4446 - 4455. [Abstract] [Full Text] [PDF]
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M. M. Fort, R. Lesley, N. J. Davidson, S. Menon, F. Brombacher, M. W. Leach, and D. M. Rennick IL-4 Exacerbates Disease in a Th1 Cell Transfer Model of Colitis J. Immunol., February 15, 2001; 166(4): 2793 - 2800. [Abstract] [Full Text] [PDF]
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G. Cai, R. Kastelein, and C. A. Hunter Interleukin-18 (IL-18) Enhances Innate IL-12-Mediated Resistance to Toxoplasma gondii Infect. Immun., December 1, 2000; 68(12): 6932 - 6938. [Abstract] [Full Text] [PDF]
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L. Fantuzzi, P. Puddu, B. Varano, M. Del Cornò, F. Belardelli, and S. Gessani IFN-{alpha} and IL-18 exert opposite regulatory effects on the IL-12 receptor expression and IL-12-induced IFN-{gamma} production in mouse macrophages: novel pathways in the regulation of the inflammatory response of macrophages J. Leukoc. Biol., November 1, 2000; 68(5): 707 - 714. [Abstract] [Full Text]
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A. Puig-Kroger, F. Sanz-Rodriguez, N. Longo, P. Sanchez-Mateos, L. Botella, J. Teixido, C. Bernabeu, and A. L. Corbi Maturation-Dependent Expression and Function of the CD49d Integrin on Monocyte-Derived Human Dendritic Cells J. Immunol., October 15, 2000; 165(8): 4338 - 4345. [Abstract] [Full Text] [PDF]
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H. Hochrein, M. O'Keeffe, T. Luft, S. Vandenabeele, R. J. Grumont, E. Maraskovsky, and K. Shortman Interleukin (Il)-4 Is a Major Regulatory Cytokine Governing Bioactive IL-12 Production by Mouse and Human Dendritic Cells J. Exp. Med., September 18, 2000; 192(6): 823 - 834. [Abstract] [Full Text] [PDF]
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P. Kalinski, H. H. Smits, J. H. N. Schuitemaker, P. L. Vieira, M. van Eijk, E. C. de Jong, E. A. Wierenga, and M. L. Kapsenberg IL-4 Is a Mediator of IL-12p70 Induction by Human Th2 Cells: Reversal of Polarized Th2 Phenotype by Dendritic Cells J. Immunol., August 15, 2000; 165(4): 1877 - 1881. [Abstract] [Full Text] [PDF]
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H. Nagayama, K. Sato, H. Kawasaki, M. Enomoto, C. Morimoto, K. Tadokoro, T. Juji, S. Asano, and T. A. Takahashi IL-12 Responsiveness and Expression of IL-12 Receptor in Human Peripheral Blood Monocyte-Derived Dendritic Cells J. Immunol., July 1, 2000; 165(1): 59 - 66. [Abstract] [Full Text] [PDF]
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E. U. Bagriacik and J. R. Klein The Thyrotropin (Thyroid-Stimulating Hormone) Receptor Is Expressed on Murine Dendritic Cells and on a Subset of CD45RBhigh Lymph Node T Cells: Functional Role for Thyroid-Stimulating Hormone During Immune Activation J. Immunol., June 15, 2000; 164(12): 6158 - 6165. [Abstract] [Full Text] [PDF]
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