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PMID |
Sentence |
1 |
15699483
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LFA-1 co-stimulation inhibits T(h)2 differentiation by down-modulating IL-4 responsiveness.
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2 |
15699483
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Specifically, CD28 co-stimulation promotes T(h)2 differentiation, whereas leukocyte function-associated antigen-1 (LFA-1) co-stimulation promotes T(h)1 differentiation and inhibits T(h)2 differentiation.
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3 |
15699483
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We show that co-stimulation through LFA-1 does not decrease early IL-4 secretion, but rather induces a loss in IL-4 responsiveness.
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4 |
15699483
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T cells primed in the context of LFA-1 co-stimulation require a 5-fold increase in the concentration of IL-4 required to drive T(h)2 differentiation, which is not mediated by a loss in IL-4R expression.
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5 |
15699483
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To determine whether LFA-1 co-stimulation impacts on proximal signaling from the IL-4R, we first identified a kinetic window where we could separate IL-4-driven T(h)2 differentiation from initial T cell priming.
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6 |
15699483
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Proximal IL-4R signaling, as evidenced by tyrosine phosphorylation of signal transducer and activator of transcription-6 (STAT6), was not inhibited by initial co-stimulation through LFA-1, yet these T cells still required higher amounts of IL-4 and corresponding higher levels of STAT6 activation to up-regulate GATA-3 and induce T(h)2 differentiation.
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7 |
15699483
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Thus, LFA-1 co-stimulation appears to interfere with GATA-3 expression downstream of STAT6.
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8 |
15699483
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These results suggest that LFA-1 co-stimulation functions as a threshold modulator of T(h)2 differentiation, increasing the effective concentration of IL-4 required to drive T(h)2 responses.
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9 |
15699483
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LFA-1 co-stimulation inhibits T(h)2 differentiation by down-modulating IL-4 responsiveness.
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10 |
15699483
|
Specifically, CD28 co-stimulation promotes T(h)2 differentiation, whereas leukocyte function-associated antigen-1 (LFA-1) co-stimulation promotes T(h)1 differentiation and inhibits T(h)2 differentiation.
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11 |
15699483
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We show that co-stimulation through LFA-1 does not decrease early IL-4 secretion, but rather induces a loss in IL-4 responsiveness.
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12 |
15699483
|
T cells primed in the context of LFA-1 co-stimulation require a 5-fold increase in the concentration of IL-4 required to drive T(h)2 differentiation, which is not mediated by a loss in IL-4R expression.
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13 |
15699483
|
To determine whether LFA-1 co-stimulation impacts on proximal signaling from the IL-4R, we first identified a kinetic window where we could separate IL-4-driven T(h)2 differentiation from initial T cell priming.
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14 |
15699483
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Proximal IL-4R signaling, as evidenced by tyrosine phosphorylation of signal transducer and activator of transcription-6 (STAT6), was not inhibited by initial co-stimulation through LFA-1, yet these T cells still required higher amounts of IL-4 and corresponding higher levels of STAT6 activation to up-regulate GATA-3 and induce T(h)2 differentiation.
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15 |
15699483
|
Thus, LFA-1 co-stimulation appears to interfere with GATA-3 expression downstream of STAT6.
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16 |
15699483
|
These results suggest that LFA-1 co-stimulation functions as a threshold modulator of T(h)2 differentiation, increasing the effective concentration of IL-4 required to drive T(h)2 responses.
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17 |
16341143
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Interestingly, the modified plasmid vaccine predominantly enhanced the type 2 immune responses manifested by an increased IgG1 to IgG2a antibody ratio and a greater induction of GATA-3 and IL-4 mRNA than that of T-bet and IFN-gamma mRNA in spleen cells from vaccinated mice.
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18 |
16341143
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In addition, protection against tumor challenge in vaccinated mice showed that there was no significant change in mice survival after in vivo CD8+CTL depletion, indicating that antitumor immunity augmented by plasmid encoding GM-CSF and target PDTRP gene vaccine was dominated by Th2 immune response.
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19 |
17086422
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We further showed that the mechanisms involved in the inhibitory effect of C3d3 might be possible due to impairing the function of antigen presenting B lymphocytes and reducing the expression of transcription factors (T-bet and GATA-3) and cytokine IL-4.
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20 |
17299718
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Immunosuppression during active tuberculosis is characterized by decreased interferon- gamma production and CD25 expression with elevated forkhead box P3, transforming growth factor- beta , and interleukin-4 mRNA levels.
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21 |
17299718
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All 3 groups displayed BCG-induced increases in effector and regulatory T cell phenotypes as defined by CD4(+)CD25(lo) and CD4(+)CD25(hi) T cells, respectively.
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22 |
17299718
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In case patients with active disease, BCG stimulation induced the lowest increase of CD25, CD4(+)CD25(hi), CTLA-4, and interferon- gamma .
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23 |
17299718
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However, these case patients expressed the highest mRNA levels of forkhead box P3, transforming growth factor (TGF)- beta , and interleukin (IL)-4 and a lower T-bet : GATA-3 ratio.
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24 |
17299718
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There were no significant differences in IL-4 delta 2, IL-10, or TGF- beta receptor-II mRNA expression between groups.
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25 |
17997199
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This Th1 shift was supported by an increased T-bet/GATA3 mRNA ratio.
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26 |
17997199
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IL-5 production within the airways was suppressed after the pretreatment with rCTB-Bet v 1, while local allergen-specific IgA antibodies were markedly enhanced by pretreatment with the construct.
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27 |
17997199
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Upregulation of Foxp3, IL-10 and TGF-beta mRNA expression was detected in splenocytes after pretreatment with unconjugated allergen but not with the fusion molecule, indicating that antigen conjugation to a mucosal carrier modifies the immunomodulating properties of an antigen/allergen.
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28 |
18056374
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Interaction between GATA-3 and the transcriptional coregulator Pias1 is important for the regulation of Th2 immune responses.
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29 |
18056374
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Here, we reported a number of GATA-3 associated proteins in Th2 cells, and one of such proteins Pias1 functioned as a positive transcriptional coregulator for GATA-3.
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30 |
18056374
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When overexpressed in Th2 cells, Pias1 enhanced the expression of IL-13, and to lesser degrees, IL-4 and -5.
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31 |
18056374
|
In Leishmania major infection, manipulating Pias1 expression in parasite-reactive CD4 T cells altered severity of disease caused by Th2 responses.
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32 |
18056374
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Mechanistically, Pias1 markedly potentiated GATA-3-mediated activation of the IL-13 promoter by facilitating the recruitment of GATA-3 to the promoter.
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33 |
18056374
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In contrast, IL-5 promoter was modestly enhanced by Pias1 and no effect was observed on IL-4 promoter.
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34 |
18056374
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Interaction between GATA-3 and the transcriptional coregulator Pias1 is important for the regulation of Th2 immune responses.
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35 |
18056374
|
Here, we reported a number of GATA-3 associated proteins in Th2 cells, and one of such proteins Pias1 functioned as a positive transcriptional coregulator for GATA-3.
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36 |
18056374
|
When overexpressed in Th2 cells, Pias1 enhanced the expression of IL-13, and to lesser degrees, IL-4 and -5.
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37 |
18056374
|
In Leishmania major infection, manipulating Pias1 expression in parasite-reactive CD4 T cells altered severity of disease caused by Th2 responses.
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38 |
18056374
|
Mechanistically, Pias1 markedly potentiated GATA-3-mediated activation of the IL-13 promoter by facilitating the recruitment of GATA-3 to the promoter.
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39 |
18056374
|
In contrast, IL-5 promoter was modestly enhanced by Pias1 and no effect was observed on IL-4 promoter.
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40 |
18056374
|
Interaction between GATA-3 and the transcriptional coregulator Pias1 is important for the regulation of Th2 immune responses.
|
41 |
18056374
|
Here, we reported a number of GATA-3 associated proteins in Th2 cells, and one of such proteins Pias1 functioned as a positive transcriptional coregulator for GATA-3.
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42 |
18056374
|
When overexpressed in Th2 cells, Pias1 enhanced the expression of IL-13, and to lesser degrees, IL-4 and -5.
|
43 |
18056374
|
In Leishmania major infection, manipulating Pias1 expression in parasite-reactive CD4 T cells altered severity of disease caused by Th2 responses.
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44 |
18056374
|
Mechanistically, Pias1 markedly potentiated GATA-3-mediated activation of the IL-13 promoter by facilitating the recruitment of GATA-3 to the promoter.
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45 |
18056374
|
In contrast, IL-5 promoter was modestly enhanced by Pias1 and no effect was observed on IL-4 promoter.
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46 |
18566382
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Coligation of the hepatitis C virus receptor CD81 with CD28 primes naive T lymphocytes to acquire type 2 effector function.
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47 |
18566382
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In this study, we describe for the first time that coligation of the tetraspanins CD81, CD82, or CD9 with the costimulatory molecule CD28 in vitro leads to proliferation of naive T cells.
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48 |
18566382
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When activated through this pathway, both CD4+ and CD8+ naive T cells differentiate into type 2 effector cells, which produce IL-4, IL-5, IL-13, and IL-10, together with IL-2 and TNF-alpha, but little to no IFN-gamma.
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49 |
18566382
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These effector cells descend from precursors that display early and strong production of IL-4, STAT6 phosphorylation, and up-regulation of the transcription factor GATA-3, suggesting a direct skewing toward Th2 differentiation without a Th0 intermediate.
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50 |
18566382
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The hepatitis C virus envelope protein E2 is the only ligand known for CD81.
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51 |
18579694
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Differential expression of interleukin-4 (IL-4) and IL-4 delta 2 mRNA, but not transforming growth factor beta (TGF-beta), TGF-beta RII, Foxp3, gamma interferon, T-bet, or GATA-3 mRNA, in patients with fast and slow responses to antituberculosis treatment.
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52 |
18579694
|
This study investigated interleukin-4 (IL-4), IL-4 delta 2, transforming growth factor beta (TGF-beta), TGF-beta RII, Foxp3, GATA-3, T-bet, and gamma interferon (IFN-gamma) transcription in peripheral blood samples of adult pulmonary tuberculosis patients prior to and after 1 week of therapy.
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53 |
18579694
|
There were no significant differences in expression of TGF-beta, TGF-beta RII, Foxp3, IFN-gamma, and GATA-3 between the groups.
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54 |
18579694
|
Differential expression of interleukin-4 (IL-4) and IL-4 delta 2 mRNA, but not transforming growth factor beta (TGF-beta), TGF-beta RII, Foxp3, gamma interferon, T-bet, or GATA-3 mRNA, in patients with fast and slow responses to antituberculosis treatment.
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55 |
18579694
|
This study investigated interleukin-4 (IL-4), IL-4 delta 2, transforming growth factor beta (TGF-beta), TGF-beta RII, Foxp3, GATA-3, T-bet, and gamma interferon (IFN-gamma) transcription in peripheral blood samples of adult pulmonary tuberculosis patients prior to and after 1 week of therapy.
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56 |
18579694
|
There were no significant differences in expression of TGF-beta, TGF-beta RII, Foxp3, IFN-gamma, and GATA-3 between the groups.
|
57 |
18579694
|
Differential expression of interleukin-4 (IL-4) and IL-4 delta 2 mRNA, but not transforming growth factor beta (TGF-beta), TGF-beta RII, Foxp3, gamma interferon, T-bet, or GATA-3 mRNA, in patients with fast and slow responses to antituberculosis treatment.
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58 |
18579694
|
This study investigated interleukin-4 (IL-4), IL-4 delta 2, transforming growth factor beta (TGF-beta), TGF-beta RII, Foxp3, GATA-3, T-bet, and gamma interferon (IFN-gamma) transcription in peripheral blood samples of adult pulmonary tuberculosis patients prior to and after 1 week of therapy.
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59 |
18579694
|
There were no significant differences in expression of TGF-beta, TGF-beta RII, Foxp3, IFN-gamma, and GATA-3 between the groups.
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60 |
20032499
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WAS(-/-) CD4(+) T cells mediated protective T-helper 1 (Th1) responses to Leishmania major in vivo, but were unable to support Th2 immunity to Nippostrongylus brasiliensis or L major.
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61 |
20032499
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WAS(-/-) CD4(+) T cells up-regulated IL-4 and GATA3 mRNA and secreted IL-4 protein during Th2 differentiation.
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62 |
20032499
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WAS(-/-) Th2s failed to produce IL-4 protein on restimulation despite elevated IL-4/GATA3 mRNA.
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63 |
20032499
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Moreover, dominant-negative WASp expression in WT effector T cells blocked IL-4 production, but had no effect on IFNgamma.
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64 |
20032499
|
WAS(-/-) CD4(+) T cells mediated protective T-helper 1 (Th1) responses to Leishmania major in vivo, but were unable to support Th2 immunity to Nippostrongylus brasiliensis or L major.
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65 |
20032499
|
WAS(-/-) CD4(+) T cells up-regulated IL-4 and GATA3 mRNA and secreted IL-4 protein during Th2 differentiation.
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66 |
20032499
|
WAS(-/-) Th2s failed to produce IL-4 protein on restimulation despite elevated IL-4/GATA3 mRNA.
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67 |
20032499
|
Moreover, dominant-negative WASp expression in WT effector T cells blocked IL-4 production, but had no effect on IFNgamma.
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68 |
20072623
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After in vitro stimulation, spleen cells of immunized mice produce high levels of Th1 cytokines and show a prominent mRNA expression of the Th1 transcription factor T-bet, in detriment of the Th2 transcription factor GATA-3.
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69 |
20072623
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Following R. equi challenge, a high H2O2, NO, IL-12, and IFN-gamma content is detected in the organs of immunized mice.
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70 |
20072623
|
On the other hand, TNF-alpha and IL-4 levels are markedly lower in the organs of vaccinated mice, compared with the non-vaccinated ones.
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71 |
20072623
|
A greater incidence of CD4+ and CD8+ T cells and B lymphocytes is verified in vaccinated mice.
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72 |
20072623
|
However, there is no difference between vaccinated and non-vaccinated mice in terms of the frequency of CD4+CD25+Foxp3+ T cells.
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73 |
20232336
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The mRNA expressions of Th1/Th2 cytokines (IFN-gamma and IL-10) and transcription factors (T-bet and GATA-3) in splenocytes were also markedly up-regulated by 1, compared with the control group immunized with rL-H5 alone (P<0.01 or P<0.001).
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74 |
20392496
|
IL-4 directs both CD4 and CD8 T cells to produce Th2 cytokines in vitro, but only CD4 T cells produce these cytokines in response to alum-precipitated protein in vivo.
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75 |
20392496
|
While IL-4 directs CD4 T cells to produce Th2 cytokines (including IL-4, IL-13, IL-5) in vitro it has been shown that production of these cytokines can be induced in vivo in the absence of IL-4/IL-13/STAT-6 signaling.
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76 |
20392496
|
The present report shows that CD8 as well as CD4 T cells activated through their TCR, in vitro upregulate the Th2-features - IL-4, IL-13, IL-5, and GATA-3.
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77 |
20392496
|
However, in vivo while alum-precipitated antigen strongly and selectively induces these Th2-features in CD4 T cells, CD8 T cells mount a markedly different response to this antigen.
|
78 |
20392496
|
This CD8 response is associated with strong proliferation and production of IFN-gamma, but no Th2-features are induced.
|
79 |
20392496
|
Alum-protein formulations are widely used in human vaccines and typically induce strong antibody responses characterized by the differentiation of IL-4-producing CD4 T cells and immunoglobulin class switching to IgG1.
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80 |
20392496
|
Analysis of the in vivo response to alum-precipitated protein shows that while subsets of CD4 T cells strongly upregulate Th2 and follicular helper T cell features including the surface markers OX40, CXCR5, PD-1, IL-17RB and the transcription factor c-Maf, CD8 T cells do not.
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81 |
20392496
|
These discrete differences between responding CD4 and CD8 T cells provide further insight into the differences between Th2 polarization of CD4 T cells directed by IL-4 in vitro and the induction of IL-4 production by CD4 T cells in vivo in response to alum-precipitated protein.
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82 |
20434553
|
Splenocytes were separated for detection of lymphocyte proliferation in responses to concanavalin A (Con A), lipopolysaccharide (LPS) and OVA, and mRNA expression of Th1 cytokines (IFN-gamma and IL-12), Th2 cytokines (IL-10 and IL-5) and transcription factors T-bet/GATA-3 (Th1/Th2 switcher).
|
83 |
20434553
|
In addition, up-regulated T-bet/GATA-3 together with significantly increased mRNA expression of IL-4, IL-10, IFN-gamma and IL-12 by splenocytes, as well as the proliferative responses of splenocytes to Con A, LPS and OVA were observed in paclitaxel-adjuvanted groups.
|
84 |
20434553
|
Incubation of a murine macrophage-like cell line with paclitaxel significantly increased TNF-alpha and -10 released from the cells and expression of microRNAs such as miR-155, miR-147, miR-146a and miR-132.
|
85 |
20434553
|
Splenocytes were separated for detection of lymphocyte proliferation in responses to concanavalin A (Con A), lipopolysaccharide (LPS) and OVA, and mRNA expression of Th1 cytokines (IFN-gamma and IL-12), Th2 cytokines (IL-10 and IL-5) and transcription factors T-bet/GATA-3 (Th1/Th2 switcher).
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86 |
20434553
|
In addition, up-regulated T-bet/GATA-3 together with significantly increased mRNA expression of IL-4, IL-10, IFN-gamma and IL-12 by splenocytes, as well as the proliferative responses of splenocytes to Con A, LPS and OVA were observed in paclitaxel-adjuvanted groups.
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87 |
20434553
|
Incubation of a murine macrophage-like cell line with paclitaxel significantly increased TNF-alpha and -10 released from the cells and expression of microRNAs such as miR-155, miR-147, miR-146a and miR-132.
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88 |
20696860
|
The differentiation of CD4(+) T cells into the Th2 subset is controlled by the transcription factor GATA-3.
|
89 |
20696860
|
We show in this study that IL-4 stimulation induces GATA-3 mRNA upregulation, but the level of GATA-3 protein induced is insufficient for Th2 differentiation.
|
90 |
20696860
|
The levels of GATA-3 protein and Th2 differentiation are enhanced by concomitant TCR signaling through the PI3K/mammalian target of rapamycin pathway.
|
91 |
20696860
|
The PI3K-mediated increase in GATA-3 protein occurs without increasing the GATA-3 mRNA level.
|
92 |
20696860
|
Rather, TCR signaling through PI3K specifically enhances the translation rate of GATA-3 without affecting the protein stability.
|
93 |
20696860
|
Thus, TCR signaling through PI3K may play a critical role in Th2 differentiation by the specific enhancement of GATA-3 translation.
|
94 |
20696860
|
The differentiation of CD4(+) T cells into the Th2 subset is controlled by the transcription factor GATA-3.
|
95 |
20696860
|
We show in this study that IL-4 stimulation induces GATA-3 mRNA upregulation, but the level of GATA-3 protein induced is insufficient for Th2 differentiation.
|
96 |
20696860
|
The levels of GATA-3 protein and Th2 differentiation are enhanced by concomitant TCR signaling through the PI3K/mammalian target of rapamycin pathway.
|
97 |
20696860
|
The PI3K-mediated increase in GATA-3 protein occurs without increasing the GATA-3 mRNA level.
|
98 |
20696860
|
Rather, TCR signaling through PI3K specifically enhances the translation rate of GATA-3 without affecting the protein stability.
|
99 |
20696860
|
Thus, TCR signaling through PI3K may play a critical role in Th2 differentiation by the specific enhancement of GATA-3 translation.
|
100 |
20696860
|
The differentiation of CD4(+) T cells into the Th2 subset is controlled by the transcription factor GATA-3.
|
101 |
20696860
|
We show in this study that IL-4 stimulation induces GATA-3 mRNA upregulation, but the level of GATA-3 protein induced is insufficient for Th2 differentiation.
|
102 |
20696860
|
The levels of GATA-3 protein and Th2 differentiation are enhanced by concomitant TCR signaling through the PI3K/mammalian target of rapamycin pathway.
|
103 |
20696860
|
The PI3K-mediated increase in GATA-3 protein occurs without increasing the GATA-3 mRNA level.
|
104 |
20696860
|
Rather, TCR signaling through PI3K specifically enhances the translation rate of GATA-3 without affecting the protein stability.
|
105 |
20696860
|
Thus, TCR signaling through PI3K may play a critical role in Th2 differentiation by the specific enhancement of GATA-3 translation.
|
106 |
20696860
|
The differentiation of CD4(+) T cells into the Th2 subset is controlled by the transcription factor GATA-3.
|
107 |
20696860
|
We show in this study that IL-4 stimulation induces GATA-3 mRNA upregulation, but the level of GATA-3 protein induced is insufficient for Th2 differentiation.
|
108 |
20696860
|
The levels of GATA-3 protein and Th2 differentiation are enhanced by concomitant TCR signaling through the PI3K/mammalian target of rapamycin pathway.
|
109 |
20696860
|
The PI3K-mediated increase in GATA-3 protein occurs without increasing the GATA-3 mRNA level.
|
110 |
20696860
|
Rather, TCR signaling through PI3K specifically enhances the translation rate of GATA-3 without affecting the protein stability.
|
111 |
20696860
|
Thus, TCR signaling through PI3K may play a critical role in Th2 differentiation by the specific enhancement of GATA-3 translation.
|
112 |
20696860
|
The differentiation of CD4(+) T cells into the Th2 subset is controlled by the transcription factor GATA-3.
|
113 |
20696860
|
We show in this study that IL-4 stimulation induces GATA-3 mRNA upregulation, but the level of GATA-3 protein induced is insufficient for Th2 differentiation.
|
114 |
20696860
|
The levels of GATA-3 protein and Th2 differentiation are enhanced by concomitant TCR signaling through the PI3K/mammalian target of rapamycin pathway.
|
115 |
20696860
|
The PI3K-mediated increase in GATA-3 protein occurs without increasing the GATA-3 mRNA level.
|
116 |
20696860
|
Rather, TCR signaling through PI3K specifically enhances the translation rate of GATA-3 without affecting the protein stability.
|
117 |
20696860
|
Thus, TCR signaling through PI3K may play a critical role in Th2 differentiation by the specific enhancement of GATA-3 translation.
|
118 |
20696860
|
The differentiation of CD4(+) T cells into the Th2 subset is controlled by the transcription factor GATA-3.
|
119 |
20696860
|
We show in this study that IL-4 stimulation induces GATA-3 mRNA upregulation, but the level of GATA-3 protein induced is insufficient for Th2 differentiation.
|
120 |
20696860
|
The levels of GATA-3 protein and Th2 differentiation are enhanced by concomitant TCR signaling through the PI3K/mammalian target of rapamycin pathway.
|
121 |
20696860
|
The PI3K-mediated increase in GATA-3 protein occurs without increasing the GATA-3 mRNA level.
|
122 |
20696860
|
Rather, TCR signaling through PI3K specifically enhances the translation rate of GATA-3 without affecting the protein stability.
|
123 |
20696860
|
Thus, TCR signaling through PI3K may play a critical role in Th2 differentiation by the specific enhancement of GATA-3 translation.
|
124 |
21079691
|
We found that the Th1 subset dominated the UGT, as IFN-γ and T-bet mRNA expression were high, while GATA-3 was low following genital infection with C. trachomatis serovar D.
|
125 |
21079691
|
By contrast, IL-10 and GATA-3 mRNA dominated the LGT, suggesting the presence of Th2 cells.
|
126 |
21079691
|
We found that the Th1 subset dominated the UGT, as IFN-γ and T-bet mRNA expression were high, while GATA-3 was low following genital infection with C. trachomatis serovar D.
|
127 |
21079691
|
By contrast, IL-10 and GATA-3 mRNA dominated the LGT, suggesting the presence of Th2 cells.
|
128 |
21469112
|
In this study, we show that, in mice, immunization with soluble, recombinant FliC protein flagellin (sFliC) induces Th2 responses as evidenced by Ag-specific GATA-3, IL-4 mRNA, and protein induction in CD62L(lo) CD4(+) T cells without associated IFN-γ production.
|
129 |
21469112
|
Salmonella infection in sFliC-immunized mice resulted in augmented Th1 responses, with greater bacterial clearance and increased numbers of IFN-γ-producing CD4(+) T cells, despite the early induction of Th2 features to sFliC.
|
130 |
21469117
|
Here, we show that IL-4 and IL-13 production is NF-κB1-dependent in mouse OVA-specific CD4(+) (OTII) T cells responding to alum-precipitated OVA (alumOVA) immunization.
|
131 |
21469117
|
More surprisingly, we found that NF-κB1 deficiency in OTII cells also selectively impairs their CXCR5 induction by alumOVA without affecting upregulation of BCL6, IL-21, OX40 and CXCR4 mRNA and PD-1 protein.
|
132 |
21469117
|
The selective effects of NF-κB1-deficiency on Th2 and follicular helper T cell induction do not appear to be due to altered expression of the Th2-associated transcription factors - GATA-3, c-Maf and Ikaros.
|
133 |
21469117
|
Altogether, these results suggest that NF-κB1 regulates the expression of CXCR5 on CD4(+) T cells primed in vivo, and thus selectively controls the T-cell-dependent germinal center component of B-cell response to alumOVA.
|
134 |
23349877
|
Genotoxic stress and RAS induce the expression of CD155, a ligand for the immune receptors DNAM-1, CD96 and TIGIT.
|
135 |
23349877
|
Induction of CD155 by Toll-like receptors depended on MYD88, TRIF and NF-κB.
|
136 |
23349877
|
Splenocytes of immunized CD155-deficient mice secreted lower levels of IL-4 and fewer IL-4 and GATA-3 expressing CD4(+) T cells were present in the spleen of Cd155(-/-) mice.
|
137 |
24273578
|
HSP70/CD80 DNA vaccine inhibits airway remodeling by regulating the transcription factors T-bet and GATA-3 in a murine model of chronic asthma.
|
138 |
24717539
|
Such NA-mediated costimulation crucially induces Th2 differentiation by suppressing T-bet expression, followed by the induction of GATA-3 and Th2 cytokines.
|
139 |
25267176
|
The expression levels of granzyme K and CD8 in DNA-vaccinated chickens were significantly (p < 0.05) higher than those in unvaccinated chickens upon IBDV challenge at 0.5 or 1 dpc.
|
140 |
25267176
|
Bursal transcripts related to innate immunity and inflammation, including TLR3, MDA5, IFN-α, IFN-β, IRF-1, IRF-10, IL-1β, IL-6, IL-8, iNOS, granzyme A, granzyme K and IL-10, were upregulated or significantly (p < 0.05) upregulated at 3 dpc and later in unvaccinated chickens challenged with IBDV.
|
141 |
25267176
|
The expression levels of genes related to immune cell regulation, apoptosis and glucose transport, including CD4, CD8, IL-2, IFN-γ, IL-12(p40), IL-18, GM-CSF, GATA-3, p53, glucose transporter-2 and glucose transporter-3, were upregulated or significantly (p < 0.05) upregulated at 3 dpc and later in unvaccinated chickens challenged with IBDV.
|
142 |
25267176
|
Taken together, the results indicate that the bursal transcriptome involved in innate immunity, inflammation, immune cell regulation, apoptosis and glucose transport, except for granzyme K and CD8, was not differentially expressed in DNA-vaccinated chickens protected from IBDV challenge.
|
143 |
25310804
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Serum antibodies were analyzed by ELISA while tissues were used to assess the expression of IgM, IgT, CD4, GATA3, FOXP3, TGF-β and IL-10 genes by quantitative PCR.
|
144 |
25310804
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This coincided with significant up-regulation of CD4 and GATA3 genes.
|
145 |
25310804
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CD4 and GATA3 mRNA expressions exhibited a similar pattern to IgT in the hindgut.
|
146 |
25310804
|
Serum antibodies were analyzed by ELISA while tissues were used to assess the expression of IgM, IgT, CD4, GATA3, FOXP3, TGF-β and IL-10 genes by quantitative PCR.
|
147 |
25310804
|
This coincided with significant up-regulation of CD4 and GATA3 genes.
|
148 |
25310804
|
CD4 and GATA3 mRNA expressions exhibited a similar pattern to IgT in the hindgut.
|
149 |
25310804
|
Serum antibodies were analyzed by ELISA while tissues were used to assess the expression of IgM, IgT, CD4, GATA3, FOXP3, TGF-β and IL-10 genes by quantitative PCR.
|
150 |
25310804
|
This coincided with significant up-regulation of CD4 and GATA3 genes.
|
151 |
25310804
|
CD4 and GATA3 mRNA expressions exhibited a similar pattern to IgT in the hindgut.
|
152 |
25424811
|
We found at the mucosal site an inhibition of the gene expression corresponding to IL-13 and Gata-3, with an induction of IFN-γ and T-bet.
|
153 |
25907170
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RpfE induces DC maturation by increasing expression of surface molecules and the production of IL-6, IL-1β, IL-23p19, IL-12p70, and TNF-α but not IL-10.
|
154 |
25907170
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This induction is mediated through TLR4 binding and subsequent activation of ERK, p38 MAPKs, and NF-κB signaling.
|
155 |
25907170
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RpfE-treated DCs effectively caused naïve CD4(+) T cells to secrete IFN-γ, IL-2, and IL-17A, which resulted in reciprocal expansions of the Th1 and Th17 cell response along with activation of T-bet and RORγt but not GATA-3.
|
156 |
26093207
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Furthermore, significant induction of TLR9, Mx and IL-1β was observed in the spleen on day 7 post-vaccination, supporting that the vaccine could trigger TLR9 signaling.
|
157 |
26093207
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Interestingly, at week 2 the ODN appeared to induce a Th1-like response, as indicated by upregulation of T-bet (a Th1 marker) and downregulation of GATA-3 (a Th2 marker).
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