BAP1 is required for homeostatic and antigen-driven expansion of peripheral T cells. BAP1 is required for homeostatic and antigen-driven expansion of peripheral.

Slides:

Advertisements

Similar presentations

MP cells, but not pathogen-elicited effector CD4+ T lymphocytes, rapidly produce IFN-γ during T. gondii infection independently of pathogen antigens. MP.

Advertisements

Donor SIRPα binding to recipient CD47 is required for triggering the innate alloresponse. Donor SIRPα binding to recipient CD47 is required for triggering.

Treg and Teff cell subsets show increased TCR overlap during colitis.

Fibroblast activation in WT and NFATc2-deficient mice.

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.

The adjMFC end point is independent of baseline titers.

Pathogenic potential of naïve Helicobacter-reactive CT6 cells in lymphopenic mice. Pathogenic potential of naïve Helicobacter-reactive CT6 cells in lymphopenic.

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.

Specific depletion of TFH and LCMV-specific CD4 T cells.

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.

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.

CD8α+ DC-deficient mice are highly susceptible to Lm infection in the absence of CD169+ macrophages. CD8α+ DC-deficient mice are highly susceptible to.

CD169+ macrophages play a critical role in mediating innate immune cell reorganization. CD169+ macrophages play a critical role in mediating innate immune.

Antitumor effect of local cancer immunotherapy treatment toward distant B16F10 tumors. Antitumor effect of local cancer immunotherapy treatment toward.

Specific depletion of CD4-DTR–derived CD4 T cells.

Splenic CD169+ macrophages express a unique gene profile.

Tfr cells’ transcriptomic profile distinguishes them from Treg and Tfh cells. Tfr cells’ transcriptomic profile distinguishes them from Treg and Tfh cells.

Localized hydrolysis of PIP2 by PLC-γ2 is mainly responsible for the PIP2 depletion inside the BCR microclusters. Localized hydrolysis of PIP2 by PLC-γ2.

FIP200 controls Bak expression via maintaining microRNA1198-5p expression. FIP200 controls Bak expression via maintaining microRNA1198-5p expression. (A)

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.

CD169+ macrophages mediate Lm translocation to the splenic T cell zones. CD169+ macrophages mediate Lm translocation to the splenic T cell zones. (A) Confocal.

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.

Identification of gene modules that predict vaccination response in young or older individuals. Identification of gene modules that predict vaccination.

Cytosolic entry of Lm required for CD8α+ DC recruitment.

NRP1-expressing myeloid cells influence adipocyte hypertrophy, development of fatty liver, and CLSs. NRP1-expressing myeloid cells influence adipocyte.

VH usage of cross-reactive B cells induced by H5N1 or H7N9 vaccination

NRP1-expressing myeloid cells contribute to adipose tissue vascularization. NRP1-expressing myeloid cells contribute to adipose tissue vascularization.

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 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.

Differential expression of TRM markers by donor- and recipient-derived T cells with time. Differential expression of TRM markers by donor- and recipient-derived.

Macrophage-resident NRP1 mitigates cytokine release and proinflammatory polarization. Macrophage-resident NRP1 mitigates cytokine release and proinflammatory.

Definition of the cellular source of IL-22.

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.

Deubiquitinating activity, but not HCF-1 binding, is required for BAP1 function in thymocytes. Deubiquitinating activity, but not HCF-1 binding, is required.

MP cells are generated from naïve cells in the periphery.

CXCR5+/+ TFH cells are essential for the generation of LCMV-neutralizing antibodies and clearance of a persistent LCMV infection. CXCR5+/+ TFH cells are.

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)

Fig. 1. MSCs undergo in vivo apoptosis after infusion without affecting immunosuppression. MSCs undergo in vivo apoptosis after infusion without affecting.

CD169+ macrophages mediate the transport of bacteria to T cell zones by trans-infecting CD8α+ DCs. CD169+ macrophages mediate the transport of bacteria.

The adjMFC end point is independent of baseline titers.

Fig. 5 A competent Fc is required for the antitumor immune response.

MP cells, but not pathogen-elicited effector CD4+ T lymphocytes, rapidly produce IFN-γ during T. gondii infection independently of pathogen antigens. MP.

Microrobots with different cell-carrying capacities under different grid lengths (lg) and burr lengths (lb). Microrobots with different cell-carrying capacities.

Platelet-released serotonin contributes to hypothermia in mice undergoing HA-hIgG–dependent anaphylaxis. Platelet-released serotonin contributes to hypothermia.

CD4+CLA+CD103+ T cells from human blood and skin share a transcriptional profile. CD4+CLA+CD103+ T cells from human blood and skin share a transcriptional.

MR1Ts recognized by the hpMR1+EC tetramer are more likely to be TRAV1-2−. MR1Ts recognized by the hpMR1+EC tetramer are more likely to be TRAV1-2−. PBMCs.

Loss of BAP1 blocks T cell differentiation at the DN3 stage in vitro.

CypD-deficient mice are susceptible to Mtb infection.

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

Tfr cells respond better to immunization with self-antigens than with foreign antigens. Tfr cells respond better to immunization with self-antigens than.

Gab3 is required for IL-2– and IL-15–induced priming and expansion of NK cells. Gab3 is required for IL-2– and IL-15–induced priming and expansion of NK.

Fig. 4 PD-L1 expression is found in the spleen and the BM of mice transplanted with JAK2V617F-transduced bone marrow. PD-L1 expression is found in the.

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.

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.

Tregs preferentially regulate TH2 cytokines in skin.

Fibroblast activation in WT and NFATc2-deficient mice.

γδ T cells producing IL-17 are required for short-term memory.

CCR6 is dispensable for expansion of innate TCRαβ+ cells in oral candidiasis. CCR6 is dispensable for expansion of innate TCRαβ+ cells in oral candidiasis.

Fig. 1 TH17 cell differentiation was severely impaired in Cxxc1-deficient mice. TH17 cell differentiation was severely impaired in Cxxc1-deficient mice.

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.

Presentation transcript:

BAP1 is required for homeostatic and antigen-driven expansion of peripheral T cells. BAP1 is required for homeostatic and antigen-driven expansion of peripheral T cells. (A) Sorted CD4+ T cells from Bap1fl/flRosa26CreERT2 or Bap1wt/wtRosa26CreERT2 mice 1 week after tamoxifen injection were transplanted into Rag2−/− recipients either separately or at a 1:1 ratio. Numbers of total splenic CD4+ T cells in recipient mice 3 weeks after transfer (n = 3 to 4) are shown. Data are representative of two independent experiments. Error bars represent SD. *P < 0.05, **P < 0.01 based on unpaired Student’s t test. (B) GSEA of WT versus KO nonpolarized, TH2, and TH17 data sets. Gene set–level heat maps (left) and FDR (right) of gene sets that are differentially enriched in WT versus KO with an FDR less than 20% are shown. (C) Number of cells recovered after 6 days of culture of naïve CD4 T cells from Bap1fl/flCd4-Cre+ (red) and Bap1wt/wtCd4-Cre+ (black) mice stimulated with anti-CD3 and anti-CD28 (n = 2). (D) Cell cycle analysis of naïve CD4 T cells from Bap1fl/flCd4-Cre+ or Bap1wt/wtCd4-Cre+ mice stimulated with anti-CD3 and anti-CD28 for 1 or 2 days (left) and proportion of cells in each phase of the cell cycle (right) (n = 3) are shown. ****P < 0.000001 based on Fisher’s exact test. (E) CellTrace-labeled naïve CD4 T cells from Bap1fl/flCd4-Cre+ or Bap1wt/wtCd4-Cre+ mice were stimulated with anti-CD3 and anti-CD28 for the indicated number of days (n = 8). CellTrace profiles (left) and number of live cells recovered (right) are shown. ****P < 0.0001 based on unpaired Student’s t test. 7-AAD, 7-aminoactinomycin D. Teresita L. Arenzana et al. Sci. Immunol. 2018;3:eaal1953 Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works