Helicobacter species induce pTreg cell differentiation during homeostasis. Helicobacter species induce pTreg cell differentiation during homeostasis. (A)

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Volume 17, Issue 1, Pages (September 2016)
MP cells, but not pathogen-elicited effector CD4+ T lymphocytes, rapidly produce IFN-γ during T. gondii infection independently of pathogen antigens. MP.
Treg and Teff cell subsets show increased TCR overlap during colitis.
MP cells are generated from naïve cells in the periphery.
Expansion of Bacteroides species during colitis does not enhance TCR-specific T cell responses. Expansion of Bacteroides species during colitis does not.
Helicobacter species induce pTreg cell differentiation during homeostasis. Helicobacter species induce pTreg cell differentiation during homeostasis. (A)
Pathogenic potential of naïve Helicobacter-reactive CT6 cells in lymphopenic mice. Pathogenic potential of naïve Helicobacter-reactive CT6 cells in lymphopenic.
Impaired development of Treg cell function upon overexpression of FOXP3A384T in naïve CD4+CD25− T cells. Impaired development of Treg cell function upon.
Immunologic responses after the MN-mediated cancer immunotherapy.
Colonic Treg TCRs (CT2 and CT6) drive Teff cell development in inflammation. Colonic Treg TCRs (CT2 and CT6) drive Teff cell development in inflammation.
LV DNA, genome, and capsid are not required for DC activation and CD8+ T cell priming in vivo. LV DNA, genome, and capsid are not required for DC activation.
FIP200 deficiency alters mitochondria activation and ROS production in T cells. FIP200 deficiency alters mitochondria activation and ROS production in.
VLPs activate DCs and antigen-specific CD8+ T cells via the STING and cGAS pathway. VLPs activate DCs and antigen-specific CD8+ T cells via the STING and.
Therapeutic effects of TIP60 allosteric modification in DSS-induced colitis. Therapeutic effects of TIP60 allosteric modification in DSS-induced colitis.
Viral fusion is required for DC activation.
Regulatory CD4+ T cell–derived IL-10 is important for B cell differentiation and the GC response. Regulatory CD4+ T cell–derived IL-10 is important for.
LV activation of DCs and subsequent CD8+ T cell priming are dependent on STING and cGAS but not on MyD88, TRIF, or MAVS. LV activation of DCs and subsequent.
Human PBMC-derived MERS-CoV–specific T cells are multifunctional.
Protection from autoimmunity is not due to the expansion of Treg subsets. Protection from autoimmunity is not due to the expansion of Treg subsets. (A.
VH usage of cross-reactive B cells induced by H5N1 or H7N9 vaccination
Transfer of NRP1-expressing bone marrow improves the metabolic phenotype of LysM-Cre-Nrp1fl/fl mice. Transfer of NRP1-expressing bone marrow improves the.
Genetic FIP200 deletion impairs autophagy induction and causes T cell apoptosis. Genetic FIP200 deletion impairs autophagy induction and causes T cell.
MP cells can mediate resistance in infectious models that induce TH1-type immunity. MP cells can mediate resistance in infectious models that induce TH1-type.
MP cells consist of rapidly proliferating CD5hi and relatively quiescent CD5lo cells, both of which require CD28 signaling for Ki67 expression. MP cells.
Tfr cells robustly secrete IL-10 after acute viral infection.
Donor and recipient BAL T cells are phenotypically and functionally memory T cells. Donor and recipient BAL T cells are phenotypically and functionally.
Differential expression of TRM markers by donor- and recipient-derived T cells with time. Differential expression of TRM markers by donor- and recipient-derived.
Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells. Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells.
Blood Tfr cells show expression of follicular and regulatory markers.
DSS + αIL10R colitis is associated with differential changes of bacterial composition in the lumen and mucosa. DSS + αIL10R colitis is associated with.
T-bethi MP cells produce IFN-γ in response to IL-12.
IL-10R-deficient macrophages secrete IL-23, inducing IL-22 secretion by ILC3 and TH17 cells. IL-10R-deficient macrophages secrete IL-23, inducing IL-22.
BAP1 deficiency results in thymic atrophy and loss of thymocyte populations. BAP1 deficiency results in thymic atrophy and loss of thymocyte populations.
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Inhibiting or altering the timing of microbial antigen encounter results in inflammatory T cell responses against gut bacteria. Inhibiting or altering.
MP cells are generated from naïve cells in the periphery.
GPR55 restrains IEL accumulation in the small intestine.
Cell viability tests. Cell viability tests. SEM images of (A) MC3T3-E1 cells and (B) MSCs on days 1, 3, and 5 of culture. (C) Survival rates of MC3T3-E1.
Tumor control by necroptotic cells requires BATF3+cDC1 and CD8+leukocytes. Tumor control by necroptotic cells requires BATF3+cDC1 and CD8+leukocytes. (A)
APCs from hypertensive mice present antigens more efficiently.
High numbers of non–islet-specific CTLs attenuate effector functions of islet-specific CTLs. High numbers of non–islet-specific CTLs attenuate effector.
Evaluation of multidonor class Ig sequences obtained from H5N1 and H7N9 vaccinated donors. Evaluation of multidonor class Ig sequences obtained from H5N1.
BAP1 is required for homeostatic and antigen-driven expansion of peripheral T cells. BAP1 is required for homeostatic and antigen-driven expansion of peripheral.
CD4+CLA+CD103+ T cells constitute a unique cell population in human blood. CD4+CLA+CD103+ T cells constitute a unique cell population in human blood. (A)
RAPTOR deficiency impairs the DN-to-DP transition in αβ T cell development. RAPTOR deficiency impairs the DN-to-DP transition in αβ T cell development.
RORα deficiency in Tregs results in exaggerated skin inflammation in response to EC sensitization. RORα deficiency in Tregs results in exaggerated skin.
Memory-biased TCRs induce weaker TCR signals than effector-biased TCRs in vitro. Memory-biased TCRs induce weaker TCR signals than effector-biased TCRs.
Loss of BAP1 blocks T cell differentiation at the DN3 stage in vitro.
CD25 surface expression and TCR signal strength predict T helper differentiation and memory potential of early effector T cells in vivo. CD25 surface expression.
BMS blocks functional responses in primary immune cells driven by IFNα
Fig. 1 Local COX-2 overexpression selectively increased the abundance and prolonged the presence of CD90+ mSSCs in the fractured bones. Local COX-2 overexpression.
Inhibiting or altering the timing of microbial antigen encounter results in inflammatory T cell responses against gut bacteria and worsened colitis upon.
GPR55 mediates lymphocyte migration inhibition via Gα13.
Human Tfr cells do not express CD25.
Fig. 2 Phenotypic analyses of Bcl11b-deficient Treg cells.
CD4+ memory T cells derived from either CD25hi or CD25lo effector cells respond robustly to secondary challenge. CD4+ memory T cells derived from either.
CD25 expression predicts effector and memory differentiation.
Colonic Treg TCRs react to MA Helicobacter species.
Tregs preferentially regulate TH2 cytokines in skin.
Blood Tfr cells are immature but are not committed in the thymus.
Impact of FRC-specific Myd88 ablation on omental FALC organization.
Meningeal γδ T cells are biased toward IL-17 production.
Meningeal γδ T cell homeostasis is independent of inflammatory signals
Fetal-derived γδ T cells infiltrate the meninges from birth.
T cell–derived IL-13 is essential for the inception of AHR.
Bb monocolonization enhances Treg population in the cLP.
Cxxc1-deficient TH17 cells exhibit a Treg cell–like expression profile
CSGG-induced iTreg cells are capable of suppressing intestinal inflammation. CSGG-induced iTreg cells are capable of suppressing intestinal inflammation.
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Helicobacter species induce pTreg cell differentiation during homeostasis. Helicobacter species induce pTreg cell differentiation during homeostasis. (A) In vivo validation of TCR reactivity to Helicobacter species. Three-week-old SPF mice were treated with ampicillin (amp) for 2 weeks via drinking water. Two days after the last treatment, H. typhlonius or H. apodemus were gavaged for a total of three times every other day. With the last gavage, congenically marked naïve CT2/CT6 Tg cells or retrovirally expressed CT9/T7-1 cells were transferred. Seven days after transfer, cLP cells were analyzed by flow cytometry for (top) the development of Treg (Foxp3+) cells (P = 0.000003, P = 0.001, P = 0.0002, P = 0.0046, Student’s t test; n = 4 and 5 for CT2, 6 and 7 for CT9, 5 for T7-1, and 3 and 5 for CT6), (middle) frequency of transferred TCR-expressing cells among the host CD4+ T cells (P = 0.0442, P = 0.021, P = 0.0046, P = 0.0705, Student’s t test; n = 4 and 5 for CT2, 6 and 7 for CT9, 5 for T7-1, and 3 and 5 for CT6), or (bottom) CTV dilution (P = 0.00000002, P = 0.0000007, Student’s t test; n = 4 and 5 for CT2 and 3 and 5 for CT6). (B) T cell response to Helicobacter in vivo is species-specific. Three-week-old SPF mice obtained from Charles River Laboratories were gavaged with H. typhlonius or H. apodemus (for a total of three times every other day). With the last gavage, congenically marked naïve CT2 and CT6 Tg cells (105 each) were cotransferred. One week after transfer, cells from the distal mesenteric lymph node (dMLN) were analyzed by flow cytometry for the frequency of transferred TCR-expressing cells among the host CD4+ T cells (left), CTV dilution (middle), or development of Treg (Foxp3+) cells (right) (n = 4, 6, and 6). Bars indicate mean ± SEM. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001. Jiani N. Chai et al. Sci. Immunol. 2017;2:eaal5068 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works