Regulation of antibacterial B cell responses in the peritoneal cavity via MyD88 signaling in FRCs. Regulation of antibacterial B cell responses in the.

Slides:

Advertisements

Similar presentations

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

Advertisements

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

MP cells are generated from naïve cells in the periphery.

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.

IFN-γ activates the fibrinolytic system.

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

Sialylated Ab-ICs promote enhanced humoral immune responses.

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.

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.

Workspace comparison of Delta robots.

Human PBMC-derived MERS-CoV–specific T cells are multifunctional.

Deficiency in myeloid-resident NRP1 affects systemic metabolism.

Platelets are required for hFcγRIIA-induced anaphylaxis.

Reduced FOXO1 expression in GC B cells from mice lacking regulatory CD4+ T cell–derived IL-10. Reduced FOXO1 expression in GC B cells from mice lacking.

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.

β-Glucans do not modulate epithelial IL-33 or AHR.

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.

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.

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.

TCR signaling is required for exhausted-like TRM cell formation and maintenance. TCR signaling is required for exhausted-like TRM cell formation and maintenance.

IFN-γ antagonizes TGF-β in vivo.

Neutrophil depletion ameliorates colitis in Cx3cr1cre:Il10rafl/fl BM chimeras. Neutrophil depletion ameliorates colitis in Cx3cr1cre:Il10rafl/fl BM chimeras.

Unchanged worm burden and microfilaremia in basophil-deficient mice compared with their basophil-competent littermates. Unchanged worm burden and microfilaremia.

NCMs regulate T cell survival in TLOs via PD-L1.

Fig. 4 The extracellular domain of sortilin is sufficient for BDNF/TrkB signaling. The extracellular domain of sortilin is sufficient for BDNF/TrkB signaling.

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)

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.

Fig. 8 Combining M7824 with radiation or chemotherapy enhances antitumor efficacy. Combining M7824 with radiation or chemotherapy enhances antitumor efficacy.

CD4+CLA+CD103+ T cells in skin and blood are clonally related.

IFN-γ activates the fibrinolytic system.

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.

Slc7a5 deficiency stimulates osteoclastogenesis in vitro.

Shared phenotype of CD4+CLA+CD103+ T cells from human blood and skin.

Dectin-1 regulates innate IL-13.

Fig. 3 NK cells are enriched in ICB-sensitive tumors in mouse models and patients and are required for response. NK cells are enriched in ICB-sensitive.

Blood Tfr cells do not show specialized humoral regulatory capacity.

Ado loss drives TNF-dependent immune evasion.

Nuclear accumulation of NFATc1 increases in Slc7a5-deficient osteoclasts. Nuclear accumulation of NFATc1 increases in Slc7a5-deficient osteoclasts. BMMs.

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.

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. 4 Administration of BMS to mice inhibits autoimmune-relevant pharmacodynamic endpoints driven by IL-12 and IFNα. Administration of BMS

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

Fig. 4 Reconstitution of MCs in KitW-sh/W-sh mice increases IL-10+ Breg cells and suppresses the CHS response. Reconstitution of MCs in KitW-sh/W-sh mice.

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

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.

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.

Impact of FRC-specific Myd88 ablation on omental FALC organization.

Mechanisms of FRC-dependent myeloid cell recruitment.

Expansion of omental FRCs and FALC remodeling after intraperitoneal exposure to bacterial antigen. Expansion of omental FRCs and FALC remodeling after.

NE cleaves and activates GSDMD.

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.

TNF-dependent communication between FALC FRCs and myeloid cells.

Circadian gene expression in ILC3s is associated with rhythmic cytokine expression. Circadian gene expression in ILC3s is associated with rhythmic cytokine.

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

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

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:

Regulation of antibacterial B cell responses in the peritoneal cavity via MyD88 signaling in FRCs. Regulation of antibacterial B cell responses in the peritoneal cavity via MyD88 signaling in FRCs. Enumeration of IgM or IgG ASCs in the omentum (A) and peritoneal cavity (B) in mice lacking MYD88 expression in FRCs or in Cre-negative littermates (Ctrl) using ELISPOT analysis at the indicated days post-intraperitoneal (p.i.) immunization with S. Typhi OmpC/F. (C) Flow cytometry–based assessment of germinal center B cells in the indicated mouse strains after OmpC/F intraperitoneal immunization. Representative dot plot analysis on day 4 after immunization (left) and time course analysis of pooled data (right). (D and E) Serum titers of S. Typhi OmpC/F-specific IgM (D) and IgG (E) antibodies on day 4 after immunization. (F to H) C57BL/6 mice were treated with CCR2-specific depleting antibody (MC-21) or isotype control antibody (isotype), and B cell responses were analyzed at day 4 after immunization. (F) Flow cytometry–based assessment of germinal center B cells and enumeration of IgM or IgG ASC in the omentum (G) and peritoneal cavity (H). (I) ASC in the omentum of the indicated bone marrow chimeric mice on day 4 after immunization with S. Typhi OmpC/F. (J) Bacterial load in blood and liver of mice lacking MYD88 expression in FRCs or in Cre-negative littermates (Ctrl) on day 4 after intraperitoneal infection with 5 × 105 CFU of attenuated S. Typhimurium. Data are shown as mean values ± SEM and are pooled from 4 to 10 mice per group from two (D to H) or three (A to C, and I and J) independent experiments; statistical analysis was performed using Student’s t test (A to H, and J) or one-way ANOVA with Dunnett’s multiple comparison test (I) with *P < 0.05, **P < 0.01, and ***P < 0.001. Christian Perez-Shibayama et al. Sci. Immunol. 2018;3:eaar4539 Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works