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.

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

Diminished suppressive potency of primary Treg clones from IPEXA384T patients. Diminished suppressive potency of primary Treg clones from IPEXA384T patients.
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.
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.
Colonic Treg TCRs (CT2 and CT6) drive Teff cell development in inflammation. Colonic Treg TCRs (CT2 and CT6) drive Teff cell development in inflammation.
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.
CD8α+ DC-deficient mice are highly susceptible to Lm infection in the absence of CD169+ macrophages. CD8α+ DC-deficient mice are highly susceptible to.
CD169+ macrophages play a critical role in mediating innate immune cell reorganization. CD169+ macrophages play a critical role in mediating innate immune.
Specific depletion of CD4-DTR–derived CD4 T cells.
Tfr cells’ transcriptomic profile distinguishes them from Treg and Tfh cells. Tfr cells’ transcriptomic profile distinguishes them from Treg and Tfh cells.
FIP200 controls Bak expression via maintaining microRNA1198-5p expression. FIP200 controls Bak expression via maintaining microRNA1198-5p expression. (A)
CD169+ macrophages mediate Lm translocation to the splenic T cell zones. CD169+ macrophages mediate Lm translocation to the splenic T cell zones. (A) Confocal.
The PIP2 metabolism–derived amplification loop accounts for the enhanced activation of B cells expressing PLAID-associated PLC-γ2 mutants at low temperature.
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.
Cytosolic entry of Lm required for CD8α+ DC recruitment.
Platelets are required for hFcγRIIA-induced anaphylaxis.
NRP1-expressing myeloid cells influence adipocyte hypertrophy, development of fatty liver, and CLSs. NRP1-expressing myeloid cells influence adipocyte.
CD4-TEMRA cells show marked clonal expansion.
Genetic FIP200 deletion impairs autophagy induction and causes T cell apoptosis. Genetic FIP200 deletion impairs autophagy induction and causes T cell.
Abundance of non–islet-specific CTLs at islets is immune-suppressive.
Tfr cells robustly secrete IL-10 after acute viral infection.
Macrophage-resident NRP1 mitigates cytokine release and proinflammatory polarization. Macrophage-resident NRP1 mitigates cytokine release and proinflammatory.
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.
Low accessibility to Ag for CTLs leads to low proliferation of effectors. Low accessibility to Ag for CTLs leads to low proliferation of effectors. Intravital.
BAP1 deficiency results in thymic atrophy and loss of thymocyte populations. BAP1 deficiency results in thymic atrophy and loss of thymocyte populations.
Ag governs CTL behavior at islets but is not required for their accumulation in large numbers. Ag governs CTL behavior at islets but is not required for.
NCMs regulate T cell survival in TLOs via PD-L1.
PD-L1 selectively marks circulating NCMs.
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.
Fig. 4 Labeling of Msmeg with DMN-Tre is fast and specific and depends on Ag85A function. Labeling of Msmeg with DMN-Tre is fast and specific and depends.
High numbers of non–islet-specific CTLs attenuate effector functions of islet-specific CTLs. High numbers of non–islet-specific CTLs attenuate effector.
CD169+ macrophages mediate the transport of bacteria to T cell zones by trans-infecting CD8α+ DCs. CD169+ macrophages mediate the transport of bacteria.
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.
CD4+CLA+CD103+ T cells in skin and blood are clonally related.
Fig. 4. Genetically engineered PD-L1
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.
Dectin-1 regulates innate IL-13.
RORα deficiency in Tregs results in exaggerated skin inflammation in response to EC sensitization. RORα deficiency in Tregs results in exaggerated skin.
CD25 expression identifies two transcriptionally distinct subsets of very early effector cells. CD25 expression identifies two transcriptionally distinct.
Memory-biased TCRs induce weaker TCR signals than effector-biased TCRs in vitro. Memory-biased TCRs induce weaker TCR signals than effector-biased TCRs.
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
Characterization of the MCs.
Human Tfr cells do not express CD25.
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.
Fig. 2 IRF8 is expressed in CD68+ macrophages after SCI.
Fig. 5. Vascularization of human liver seed grafts.
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.
Chronic Treg reduction exacerbates bleomycin-induced skin fibrosis.
CAR expression promotes tonic activation of signaling networks.
Human basophils are unresponsive to contact-dependent or contact-independent inhibition by Tregs. Human basophils are unresponsive to contact-dependent.
Blood Tfr cells are immature but are not committed in the thymus.
Fig. 3 Characterization of SGN responses to optogenetic stimulation.
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.
Fetal-derived γδ T cells infiltrate the meninges from birth.
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.
CSGG-induced iTreg cells are capable of suppressing intestinal inflammation. CSGG-induced iTreg cells are capable of suppressing intestinal inflammation.
Presentation transcript:

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 to D) Flow plots showing similar representation of CD4+ T cells at islets in the two scenarios (A and B) but different amounts of CD8+ T cells (C and D). (E) Despite having lower amounts of total CD8+ T cells, LO mice had more islet-specific P14 T cells in the pancreas. (F and G) The distributions of Ag specificity of the CD8+ T cells present in the pancreas are visualized in (F) and (G), where each dot represents 1of 100. (H and I) Representative fixed, frozen tissue sections from HI and LO pancreata displaying the TCR-tg cells [red, P14 (islet-specific); green, OT-I (non–islet-specific)] and endogenous CD8+ T cells [blue, anti-CD8 monoclonal antibody (mAb) (polyclonal)] in islets (dashed lines). Scale bar, 20 μm. (J to L) CD4+/CD25+/FoxP3+ Treg fractions were not different between the two scenarios. (M and N) The abundant population of non–islet-specific T cells in the HI scenario had not transformed into a CD8+ Treg type as judged by the expression of FoxP3 (M) and CD122 (N). Groups are representative of at least three independent experiments. Data are means ± SEM. *P < 0.05, two-tailed unpaired Mann-Whitney U tests. MFI, mean fluorescence intensity. Gustaf Christoffersson et al. Sci. Immunol. 2018;3:eaam6533 Copyright © 2018 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works