Genetic FIP200 deletion impairs autophagy induction and causes T cell apoptosis. Genetic FIP200 deletion impairs autophagy induction and causes T cell.

Slides:



Advertisements
Similar presentations
High-dimensional analysis of lymphoid CD4+ T cells identified distinct TFH cell subsets in HIV+ patients and HCs. High-dimensional analysis of lymphoid.
Advertisements

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.
FIP200 loss links to poor autophagy and high apoptosis in naïve T cells in tumor. FIP200 loss links to poor autophagy and high apoptosis in naïve T cells.
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.
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.
FIP200 maintains microRNA1198-5p expression via Ago2 in naïve T cells.
Specific depletion of CD4-DTR–derived CD4 T cells.
CCR2+ monocytes are a relevant source of type I IFN in response to Af.
FIP200 controls Bak expression via maintaining microRNA1198-5p expression. FIP200 controls Bak expression via maintaining microRNA1198-5p expression. (A)
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.
FIP200 loss links to poor autophagy and high apoptosis in naïve T cells in tumor. FIP200 loss links to poor autophagy and high apoptosis in naïve T cells.
Human PBMC-derived MERS-CoV–specific T cells are multifunctional.
Resistance of CD141+ DCs to influenza virus in vivo in humanized mice.
Cytosolic entry of Lm required for CD8α+ DC recruitment.
Virus-specific T cell responses are detected in all MERS survivors.
Arp2/3-mediated formation of nuclear actin networks is essential for CD4+ T cell effector functions. Arp2/3-mediated formation of nuclear actin networks.
Protection from autoimmunity is not due to the expansion of Treg subsets. Protection from autoimmunity is not due to the expansion of Treg subsets. (A.
Platelets are required for hFcγRIIA-induced anaphylaxis.
VH usage of cross-reactive B cells induced by H5N1 or H7N9 vaccination
Human cells produce type I and III IFNs upon Af stimulation.
Transfer of NRP1-expressing bone marrow improves the metabolic phenotype of LysM-Cre-Nrp1fl/fl mice. Transfer of NRP1-expressing bone marrow improves the.
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.
Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells. Neutrophil recruitment to the colonic lamina propria depends on CD4+ T cells.
Blood Tfr cells show expression of follicular and regulatory markers.
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.
The mucosal environment regulates CD160 expression on IELs
Blood Tfr cells are indicators of ongoing humoral activity.
Helicobacter species induce pTreg cell differentiation during homeostasis. Helicobacter species induce pTreg cell differentiation during homeostasis. (A)
Inhibiting or altering the timing of microbial antigen encounter results in inflammatory T cell responses against gut bacteria. Inhibiting or altering.
MP cells are generated from naïve cells in the periphery.
GPR55 restrains IEL accumulation in the small intestine.
FIP200 maintains microRNA1198-5p expression via Ago2 in naïve T cells.
CXCR5+/+ TFH cells are essential for the generation of LCMV-neutralizing antibodies and clearance of a persistent LCMV infection. CXCR5+/+ TFH cells are.
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.
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.
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.
Loss of BAP1 blocks T cell differentiation at the DN3 stage in vitro.
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. 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. 5 Treatment with BMS (PO BID) protects from wasting and colitis in two SCID mouse models. Treatment with BMS (PO BID) protects from.
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.
Tfr cells respond better to immunization with self-antigens than with foreign antigens. Tfr cells respond better to immunization with self-antigens than.
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.
Human Tfr cells do not express CD25.
CD25 expression predicts effector and memory differentiation.
Pharmacological targeting of CDs promotes response to KRASG12C inhibition in vivo. Pharmacological targeting of CDs promotes response to KRASG12C inhibition.
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.
Treg expression of Gata3 plays a major role in controlling dermal fibrosis. Treg expression of Gata3 plays a major role in controlling dermal 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.
miR-146a is highly expressed selectively on γδ27− T cells.
IL-33 is not critical for initiation of allergic airways disease phenotype. IL-33 is not critical for initiation of allergic airways disease phenotype.
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.
Fetal-derived γδ T cells infiltrate the meninges from birth.
In response to allergen, T cells and ILCs are equally important sources of IL-13. In response to allergen, T cells and ILCs are equally important sources.
T cell–derived IL-13 is essential for the inception of AHR.
Presentation transcript:

Genetic FIP200 deletion impairs autophagy induction and causes T cell apoptosis. Genetic FIP200 deletion impairs autophagy induction and causes T cell apoptosis. (A) FIP200 protein expression in T cell subsets and non–T cells from Fip200flox/floxCd4+/+ (WT), Cd4c/+, and Cd4c/c (KO) mice (n = 3). (B and C) Spontaneous apoptosis of naïve T cells in WT and Fip200−/− mice. (B) Numbers on the dot plots represent the percentage of Annexin V+ naïve T cells in lymph nodes. (C) The percentages of CD4+ and CD8+ Annexin V+ naïve T cells are shown (n = 5, means ± SEM). *P < 0.05 (Mann-Whitney U tests). (D and E) Apoptosis of cultured or activated T cells in WT and Fip200−/− mice. Naïve lymph node T cells were cultured for 24 and 48 hours without (D) or with (E) anti-CD3 and anti-CD28 antibodies. Numbers on the dot plots represent the percentage of Annexin V+ T cells (n = 4, means ± SEM). *P < 0.05 (Mann-Whitney U tests). (F) The percentage of T cell subsets in lymph nodes (LNs; n = 6), spleen (SP; n = 5 to 7), bone marrow (BM; n = 3), and peripheral blood (PB; n = 3) in WT and Fip200−/− mice. *P < 0.05 (Mann-Whitney U tests). (G) Absolute numbers of T cell subsets in spleen from WT and Fip200−/− mice (n = 13, means ± SEM). *P < 0.05 (Mann-Whitney U tests). (H and I) WT CD45.1+ T cells and Fip200−/− CD45.2+ T cells were transferred into Rag1−/− mice with a 1:1 ratio. Live (H) and apoptotic (I) T cells were analyzed on day 14 in the lymph nodes and spleen in Rag1−/− mice. Numbers on the dot plots represent the percentage of CD45.1+ and CD45.2+ T cells in total T cells (H) and the percentage of Annexin V+ T cells in WT and Fip200−/− (KO) T cells (I) (n = 7). (J) Autophagy flux in T cells isolated from lymph nodes of WT and KO mice with or without TCR engagement for 24 hours. These T cells were treated with Baf for the last 4 hours to inhibit the autophagosome degradation (n = 3). (K) Expression of autophagy receptor p62 and NDP52 in fresh WT and Fip200−/− naïve T cell subsets (n = 3). Houjun Xia et al. Sci. Immunol. 2017;2:eaan4631 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works