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.

Slides:

Advertisements

Similar presentations

Fig. 3. Activation and Th1 differentiation of the P25 TCR-Tg CD4+ T cells after BCG lung infection. The N-P25 TCR-Tg mice were i.t.

Advertisements

Identification of combination treatment–responsive effector/memory tumor-infiltrating CD8+ T cell population. Identification of combination treatment–responsive.

Identification of combination treatment–responsive dysfunctional tumor-infiltrating CD8+ T cell population. Identification of combination treatment–responsive.

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.

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.

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.

CXCR5+/+ TFH cells are dispensable for maintenance of the LCMV-specific antibody response. CXCR5+/+ TFH cells are dispensable for maintenance of the LCMV-specific.

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

Memory CD8+ T cells that become terminally differentiated by multiple antigen encounters lose core 2 O-glycan synthesis activity. Memory CD8+ T cells that.

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.

Virus-specific T cell responses are detected in all MERS survivors.

Role of TLR signaling in hY4-induced changes and effects of TLR inhibition. Role of TLR signaling in hY4-induced changes and effects of TLR inhibition.

Arp2/3-mediated formation of nuclear actin networks is essential for CD4+ T cell effector functions. Arp2/3-mediated formation of nuclear actin networks.

Human cells produce type I and III IFNs upon Af stimulation.

Nonredundant antigen presentation by CD1c+ DCs infected with HIV and influenza virus. Nonredundant antigen presentation by CD1c+ DCs infected with HIV.

Volume 16, Issue 12, Pages (September 2016)

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.

DC subset cooperation for activation of antiviral T cells.

Donor and recipient BAL T cells are phenotypically and functionally memory T cells. Donor and recipient BAL T cells are phenotypically and functionally.

Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells. Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells.

T-bethi MP cells produce IFN-γ in response to IL-12.

Fig. 6 In utero injection of inflammatory cytokines or adoptive transfer of activated T cells leads to pregnancy loss. In utero injection of inflammatory.

BAP1 deficiency results in thymic atrophy and loss of thymocyte populations. BAP1 deficiency results in thymic atrophy and loss of thymocyte populations.

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)

Antigen-specific immune responses are enhanced in hypertension.

APCs from hypertensive mice present antigens more efficiently.

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

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

Members of IL-1 family of cytokines favor the generation of IL-3–secreting CD4+ T cells in vitro. Members of IL-1 family of cytokines favor the generation.

Detection of neoantigen-specific T cell recognition in cancer.

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.

CD25 expression identifies two transcriptionally distinct subsets of very early effector cells. CD25 expression identifies two transcriptionally distinct.

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.

Detection of GPR55 ligand in the small intestine.

Fig. 3 BMS blocks functional responses in primary immune cells driven by IL-23 and IL-12. BMS blocks functional responses in primary immune.

Fig. 2 In situ vaccination of CpG in combination with anti-OX40 antibody cures established local and distant tumors. In situ vaccination of CpG in combination.

BMS blocks functional responses in primary immune cells driven by IFNα

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.

Type I and III IFNR expression on hematopoietic cells is required for protection against IA. Type I and III IFNR expression on hematopoietic cells is required.

MR1Ts respond to microbially derived ligands loaded on hpMR1 tetramers

Sustained T follicular helper cell response is essential for control of chronic viral infection by Ute Greczmiel, Nike Julia Kräutler, Alessandro Pedrioli,

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.

Human basophils are unresponsive to contact-dependent or contact-independent inhibition by Tregs. Human basophils are unresponsive to contact-dependent.

Fig. 7 BEL immune response.

Lin28b promotes the positive selection of CD5+ ImmB cells in neonatal mice. Lin28b promotes the positive selection of CD5+ ImmB cells in neonatal mice.

IL-9–expressing TH cells are highly enriched in CCR4+/CCR8+ effector memory TH cells. IL-9–expressing THcells are highly enriched in CCR4+/CCR8+effector.

Acute circadian disruption alters ILC3 cytokine secretion.

REV-ERBα deficiency reduces frequency and number of NKp46+ ILC3s.

Meningeal γδ T cells are biased toward IL-17 production.

Fetal-derived γδ T cells infiltrate the meninges from birth.

Fig. 2 Cxxc1 deficiency restricts T cell–mediated autoimmunity and increases sensitivity to C. rodentium infection. Cxxc1 deficiency restricts T cell–mediated.

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

Presentation transcript:

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 T-bet+ population. (A) MP cells established in Rag γc KO mice do not contain a major Toxoplasma antigen AS15-specific population. Wild-type and Rag γc KO mice that had received CD4+ T cells 4 weeks earlier were infected with T. gondii or left uninfected, and 7 days later, CD4+ T lymphocytes from the PC and spleen of these animals were analyzed for CD44 expression and AS15 tetramer binding. The representative plots depict CD44 expression and AS15 tetramer binding for each group, whereas the bar graphs show the number (mean ± SD) of naïve, CD44hi, and CD44hi AS15 tetramer+ cells (n = 5). Data are representative of two independent experiments. (B) MP cells generated in Rag γc KO mice express T-bet. The histograms show T-bet expression by MP cells generated in Rag γc KO mice, as shown in (A). Filled histograms show negative control staining. Representative data from three animals were analyzed. (C) MP cells established in Rag γc KO mice do not produce IFN-γ in response to Toxoplasma antigen stimulation. Wild-type and Rag γc KO mice reconstituted with MP cells, as shown in (A), were infected with T. gondii, and on day 7 after infection, whole splenocytes and sorted CD44hi CD62Llo CD4+ T cells from the indicated groups were stimulated with medium, anti-CD3 mAb, STAg, or AS15 peptide in vitro. The graph indicates the concentration (mean ± SD) of IFN-γ in the culture supernatant from each group (n = 5). Data are representative of two independent experiments performed. *P < 0.05, **P < 0.01, ***P < 0.001. Takeshi Kawabe et al. Sci. Immunol. 2017;2:eaam9304 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.