Bacterial antigen encounter occurs during a specific preweaning interval, is dependent on GCs, and correlates with the presence of colonic GAPs. Bacterial.

Slides:



Advertisements
Similar presentations
Diminished suppressive potency of primary Treg clones from IPEXA384T patients. Diminished suppressive potency of primary Treg clones from IPEXA384T patients.
Advertisements

Fibroblast activation in WT and NFATc2-deficient mice.
Expansion of Bacteroides species during colitis does not enhance TCR-specific T cell responses. Expansion of Bacteroides species during colitis does not.
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.
Colonic Treg TCRs (CT2 and CT6) drive Teff cell development in inflammation. Colonic Treg TCRs (CT2 and CT6) drive Teff cell development in inflammation.
FIP200 deficiency alters mitochondria activation and ROS production in T cells. FIP200 deficiency alters mitochondria activation and ROS production in.
MP cells established in Rag γc KO mice are Toxoplasma antigen–unspecific T-bet+ population. MP cells established in Rag γc KO mice are Toxoplasma antigen–unspecific.
Specific depletion of CD4-DTR–derived CD4 T cells.
Three different types of transfer functions with a codomain of [0,1].
Memory CD8+ T cells that become terminally differentiated by multiple antigen encounters lose core 2 O-glycan synthesis activity. Memory CD8+ T cells that.
Increased resistance of GPR55-deficient mice to indomethacin-induced intestinal permeability. Increased resistance of GPR55-deficient mice to indomethacin-induced.
Ex vivo testing of the soft robotic devices.
Human PBMC-derived MERS-CoV–specific T cells are multifunctional.
Virus-specific T cell responses are detected in all MERS survivors.
Arp2/3-mediated formation of nuclear actin networks is essential for CD4+ T cell effector functions. Arp2/3-mediated formation of nuclear actin networks.
Summary of time-limited events in early life promoting tolerance to gut bacterial antigens. Summary of time-limited events in early life promoting tolerance.
Genetic FIP200 deletion impairs autophagy induction and causes T cell apoptosis. Genetic FIP200 deletion impairs autophagy induction and causes T cell.
β-Glucans do not modulate epithelial IL-33 or AHR.
Abundance of non–islet-specific CTLs at islets is immune-suppressive.
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.
Tfr cells robustly secrete IL-10 after acute viral infection.
Tfr cell–derived IL-10 is important for B cell differentiation and the GC response. Tfr cell–derived IL-10 is important for B cell differentiation and.
EGFR activation in GCs inhibits GAP formation and luminal antigen delivery throughout life. EGFR activation in GCs inhibits GAP formation and luminal antigen.
Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells. Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells.
Definition of the cellular source of IL-22.
Donor TRM persistence is associated with reduced clinical complications. Donor TRM persistence is associated with reduced clinical complications. Patient.
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.
The microbiota inhibits colonic GAPs and antigen delivery after weaning. The microbiota inhibits colonic GAPs and antigen delivery after weaning. (A) Expression.
Inhibiting or altering the timing of microbial antigen encounter results in inflammatory T cell responses against gut bacteria. Inhibiting or altering.
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)
Antigen-specific immune responses are enhanced in hypertension.
APCs from hypertensive mice present antigens more efficiently.
BAP1 is required for homeostatic and antigen-driven expansion of peripheral T cells. BAP1 is required for homeostatic and antigen-driven expansion of peripheral.
Ado loss alters cellular metabolism.
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.
CD4+CLA+CD103+T cells from human blood and skin share a functional profile. CD4+CLA+CD103+T cells from human blood and skin share a functional profile.
Shared phenotype of CD4+CLA+CD103+ T cells from human blood and skin.
Dynamic regulation of cell metabolism and mTORC1 activity and the requirement of RAPTOR in thymocyte development. Dynamic regulation of cell metabolism.
RORα deficiency in Tregs results in exaggerated skin inflammation in response to EC sensitization. RORα deficiency in Tregs results in exaggerated skin.
Loss of BAP1 blocks T cell differentiation at the DN3 stage in vitro.
CypD-deficient mice are susceptible to Mtb infection.
Fig. 3. Increased expression of exhaustion markers and apoptosis markers on CAR8 cells in the presence of TCR antigen. Increased expression of exhaustion.
Fig. 1. CAR4 and CAR8 cells demonstrate in vitro and in vivo antileukemic efficacy. CAR4 and CAR8 cells demonstrate in vitro and in vivo antileukemic efficacy.
CD25 surface expression and TCR signal strength predict T helper differentiation and memory potential of early effector T cells in vivo. CD25 surface expression.
Detection of GPR55 ligand in the small intestine.
In vitro cell-release experiments on a glass substrate.
Tfr cells respond better to immunization with self-antigens than with foreign antigens. Tfr cells respond better to immunization with self-antigens than.
Inhibiting or altering the timing of microbial antigen encounter results in inflammatory T cell responses against gut bacteria and worsened colitis upon.
Fig. 2 Phenotypic analyses of Bcl11b-deficient Treg cells.
Fig. 3 Local Maraba treatment of TNBC tumors provides long-term systemic protection. Local Maraba treatment of TNBC tumors provides long-term systemic.
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.
Immune evasion occurs independently of perforin-mediated killing.
GPR55 regulates γδT cell egress from PP and homing of gut-tropic CD8 T cells to the small intestine. GPR55 regulates γδT cell egress from PP and homing.
Treg expression of Gata3 plays a major role in controlling dermal fibrosis. Treg expression of Gata3 plays a major role in controlling dermal fibrosis.
miR-146a is highly expressed selectively on γδ27− T cells.
Fibroblast activation in WT and NFATc2-deficient mice.
Expansion of omental FRCs and FALC remodeling after intraperitoneal exposure to bacterial antigen. Expansion of omental FRCs and FALC remodeling after.
Lin28b promotes the positive selection of CD5+ ImmB cells in neonatal mice. Lin28b promotes the positive selection of CD5+ ImmB cells in neonatal mice.
Meningeal γδ T cell homeostasis is independent of inflammatory signals
In response to allergen, T cells and ILCs are equally important sources of IL-13. In response to allergen, T cells and ILCs are equally important sources.
Bb monocolonization enhances Treg population in the cLP.
CCR6 is dispensable for expansion of innate TCRαβ+ cells in oral candidiasis. CCR6 is dispensable for expansion of innate TCRαβ+ cells in oral candidiasis.
CSGG-induced iTreg cells are capable of suppressing intestinal inflammation. CSGG-induced iTreg cells are capable of suppressing intestinal inflammation.
Presentation transcript:

Bacterial antigen encounter occurs during a specific preweaning interval, is dependent on GCs, and correlates with the presence of colonic GAPs. Bacterial antigen encounter occurs during a specific preweaning interval, is dependent on GCs, and correlates with the presence of colonic GAPs. (A) Fold increase in CBir1 T cells after ex vivo culture with LP-MNPs isolated from the SI or colon on DOL7, DOL14, DOL21, or DOL28. (B) Percentage of (CD45.1+) CBir1 T cells of the total CD4+ T cells or (C) percentage of proliferating CBir1 T cells of the total CD45.1+ CBir1 T cells within the SI- or colon-draining MLNs 3 days after transfer into recipient CD45.2 mice on DOL7, DOL17, or DOL27. (D) Percentage of (CD45.1+) DP1 T cells of the CD4+ T cells within the MLNs 3 days after transfer. (E) Percentage of CD45.1 cells of the total CD4+CD3+ T cell population or (F) percentage of Foxp3+ cells of the CD45.1+ cells in the colon LP 7 days after transfer of CD45.1+ CBir1, DP1, or OTII T cells into recipient mice not receiving OVA. (G) Percentage of LP-MNPs staining for luminally administered Ova-647 on DOL7, DOL14, DOL21, or DOL28. (H) FITC-dextran (4 kDa) in serum after gavage in DOL18 GC knockout and littermate control mice. (I) Percentage of LP-MNPs staining for luminally administered Ova-647 in DOL18 GC knockout and littermate control mice. (J) Percentage of CD45.1+ CBir1 cells of CD4+ T cells within the MLNs 3 days after transfer into DOL18 GC knockout and littermate control mice. (K) Ratio of GAPs per GC in the SI and colon from DOL7 to DOL60. *P < 0.001; ns, not significant; n = 4 mice per group. Experiments in (B), (C), (G), (H), and (K) were repeated two independent times. Kathryn A. Knoop et al. Sci. Immunol. 2017;2:eaao1314 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works