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.

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

Volume 25, Issue 11, Pages (November 2017)
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.
Pathogenic potential of naïve Helicobacter-reactive CT6 cells in lymphopenic mice. Pathogenic potential of naïve Helicobacter-reactive CT6 cells in lymphopenic.
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.
Volume 21, Issue 7, Pages (November 2017)
DKO CD8+ T cells demonstrate a strong effector response but altered memory differentiation and maintenance after LCMV infection. DKO CD8+ T cells demonstrate.
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.
Specific depletion of CD4-DTR–derived CD4 T cells.
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.
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.
Volume 37, Issue 5, Pages (November 2012)
Human PBMC-derived MERS-CoV–specific T cells are multifunctional.
Arp2/3-mediated formation of nuclear actin networks is essential for CD4+ T cell effector functions. Arp2/3-mediated formation of nuclear actin networks.
VH usage of cross-reactive B cells induced by H5N1 or H7N9 vaccination
Nonredundant antigen presentation by CD1c+ DCs infected with HIV and influenza virus. Nonredundant antigen presentation by CD1c+ DCs infected with HIV.
Genetic FIP200 deletion impairs autophagy induction and causes T cell apoptosis. Genetic FIP200 deletion impairs autophagy induction and causes T cell.
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.
Persistent TCR–pMHC-I signaling drives the formation and maintenance of exhausted-like TRM cells. Persistent TCR–pMHC-I signaling drives the formation.
Volume 38, Issue 6, Pages (June 2013)
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.
Immune cell recruitment after the NIR-boosted and MN-mediated cancer immunotherapy. Immune cell recruitment after the NIR-boosted and MN-mediated cancer.
MP cells are generated from naïve cells in the periphery.
GPR55 restrains IEL accumulation in the small intestine.
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.
High numbers of non–islet-specific CTLs attenuate effector functions of islet-specific CTLs. High numbers of non–islet-specific CTLs attenuate effector.
Non–viral Ag–specific CTLs dampen inflammation in a mouse model of viral meningitis. Non–viral Ag–specific CTLs dampen inflammation in a mouse model of.
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.
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.
IL-27 induces expression of multiple IR by CD8+ T cells.
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.
Fig. 3 BMS blocks functional responses in primary immune cells driven by IL-23 and IL-12. BMS blocks functional responses in primary immune.
BMS blocks functional responses in primary immune cells driven by IFNα
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
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.
MDSC-derived IL-6 enhances tumor progression through the inhibition of tumor-specific TH1 development and of their helper activity for CD8+ T cells. MDSC-derived.
Human basophils are unresponsive to contact-dependent or contact-independent inhibition by Tregs. Human basophils are unresponsive to contact-dependent.
Bacterial antigen encounter occurs during a specific preweaning interval, is dependent on GCs, and correlates with the presence of colonic GAPs. Bacterial.
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.
Regulation of antibacterial B cell responses in the peritoneal cavity via MyD88 signaling in FRCs. Regulation of antibacterial B cell responses in the.
Acute circadian disruption alters ILC3 cytokine secretion.
Circadian gene expression in ILC3s is associated with rhythmic cytokine expression. Circadian gene expression in ILC3s is associated with rhythmic cytokine.
Meningeal γδ T cells are biased toward IL-17 production.
Fig. 2 Cxxc1 deficiency restricts T cell–mediated autoimmunity and increases sensitivity to C. rodentium infection. Cxxc1 deficiency restricts T cell–mediated.
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.
Presentation transcript:

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 immunity. (A to G) MP cells ameliorate toxoplasmosis via the IL-12–IFN-γ axis in the absence of pathogen antigen recognition. (A) Survival of T. gondii–infected wild-type, Rag γc KO, and Rag γc KO animals that had received CD4+ T cells from wild-type, IFN-γ KO, or IL-12Rβ2 KO mice 4 weeks earlier was monitored daily (n = 4 to 5). (B) T. gondii–infected Rag γc KO and Rag γc KO mice with MP cells were treated with anti–I-Aβ mAb or control IgG, and survival was assessed (n = 9 to 10). (C) Relative pathogen load (mean ± SD) and (D) concentration of IFN-γ in PC of T. gondii–infected wild-type, Rag γc KO, and Rag γc KO animals that received CD4+ T cells 4 weeks earlier (n = 3 to 10). AU, arbitrary units. (E and F) Serum IFN-γ and IL-12p70 concentration (mean ± SD) at the indicated days after infection (n = 3 to 5). (G) T. gondii–infected Rag γc KO mice with or without MP cells from wild-type or IFN-γ KO mice were treated with IL-12, and survival was assessed (n = 7 to 8). Data are representative of two (A and D to F), pooled from two (B and C), and pooled from three (G) independent experiments performed. (H to J) IFN-γ produced by MP cells augments antigen-specific effector CD4+ T cell responses. (H) Experimental design. Rag γc KO mice that had received CD4+ T cells from wild-type or IFN-γ KO mice at day −28 were infected with T. gondii at day 0 and transferred with sorted naïve CD4+ T cells from CD45.1 mice at day 1. (I) The representative dot plots show CD44 expression versus AS15 tetramer staining by CD45.1 donor cells from each group at day 8, whereas the bar graphs show the number (mean ± SD) of CD44hi CD45.1 donor cells (left) and the frequency (mean ± SD) of CD44hi AS15 tetramer+ cell population among CD45.1 donor cells (right; n = 5). (J) CD44hi CD62Llo CD45.1 donor cell population sorted from splenocytes of each group was stimulated with STAg. The bar graph shows the concentration (mean ± SD) of IFN-γ in the culture supernatant from each group (n = 4 to 5). (K and L) MP cells produce IFN-γ and control bacterial growth in M. bovis BCG infection. Wild-type, Rag KO, and Rag KO mice that had received CD4+ T cells 4 weeks earlier were infected with M. bovis BCG, and (K) bacterial burden (CFU; mean ± SD) in the indicated organs and (L) concentration (mean ± SD) of IFN-γ in the spleen were analyzed 17 days after infection (n = 4 to 5). (M) MP cells are protective in M. tuberculosis infection. Wild-type, Rag KO, and Rag KO mice that had received CD4+ T cells were infected with M. tuberculosis, and survival was assessed (n = 5). *P < 0.05, **P < 0.01, ***P < 0.001. NS, not significant. 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.