TNF-dependent communication between FALC FRCs and myeloid cells.

Slides:

Advertisements

Similar presentations

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

Advertisements

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

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.

Three different types of transfer functions with a codomain of [0,1].

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.

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.

Deficiency in myeloid-resident NRP1 affects systemic metabolism.

Platelets are required for hFcγRIIA-induced anaphylaxis.

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

Comparison of repertoire distributions to baseline.

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.

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.

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

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

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

Immune cell recruitment after the NIR-boosted and MN-mediated cancer immunotherapy. Immune cell recruitment after the NIR-boosted and MN-mediated cancer.

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

PD-L1 selectively marks circulating NCMs.

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

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.

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.

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

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

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

NK cell immune evasion occurs through loss of TNF pathway members.

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.

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

Dectin-1 regulates innate IL-13.

Blood Tfr cells do not show specialized humoral regulatory capacity.

Ado loss drives TNF-dependent immune evasion.

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.

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.

Fig. 3 Local Maraba treatment of TNBC tumors provides long-term systemic protection. Local Maraba treatment of TNBC tumors provides long-term systemic.

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.

Chronic Treg reduction results in dermal fibrosis.

Tregs preferentially regulate TH2 cytokines in skin.

Chronic Treg reduction exacerbates bleomycin-induced skin fibrosis.

Anti-CD40 activates TAMs and recruits inflammatory monocytes.

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.

Fig. 2. Mechanism of PD-L1 down-regulation in NOD HSPCs.

Fig. 7 Differences in the tumor microenvironment between transplant and transgenic BRAFV600E-driven melanoma models may underlie refractoriness of iBIP2.

Fig. 4 Spatial mapping of the distribution and intensity of industrial fishing catch. Spatial mapping of the distribution and intensity of industrial fishing.

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

Fig. 2 Induction and waning kinetics of merozoite-specific IgM during naturally acquired P. falciparum malaria. Induction and waning kinetics of merozoite-specific.

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 cell homeostasis is independent of inflammatory signals

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:

TNF-dependent communication between FALC FRCs and myeloid cells. TNF-dependent communication between FALC FRCs and myeloid cells. C57BL/6 (B6) (A, B, and E to G) or Cc19-EYFP (C and D) mice were treated with the indicated fusion proteins 1 day before immunization with S. Typhi OmpC/F. (A and B) Accumulation of CD11b+F4/80−Ly6G−Ly6C+ inflammatory monocytes in the omentum; relative frequency (A) and absolute numbers (B) of inflammatory monocytes in the omentum. (C) Frequency of PDPN+EYFP+ cells in the omentum after TNFR-Ig treatment as determined by flow cytometric analysis. (D) Number of FALCs per square millimeter (left) and percentage of FALC-covered area in the omentum (right). Enumeration of IgM and IgG ASCs in the omentum (E) and the peritoneal cavity (F) and flow cytometry–based analysis of germinal center–like B cells (G) on day 4 after immunization in TNFR-Ig-treated mice. (H to K) Assessment of CD11b+ myeloid cell (H) and inflammatory monocyte recruitment (I) and accumulation of germinal center B cells (J) and IgG-producing B cells (K) in the omentum of the indicated bone marrow chimeric mice on day 4 after S. Typhi OmpC/F immunization. Data are shown as mean values ± SEM and are pooled from 7 to 8 mice from three independent experiments (B, C, and E to G), from 4 to 6 mice from two independent experiments (C and D), and from 7 to 12 mice from three independent experiments (H to K); statistical analysis was performed using Student’s t test (C to G) or one-way ANOVA with Dunnett’s multiple comparison test (A, B, and H to K) 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