Diminished suppressive potency of primary Treg clones from IPEXA384T patients. Diminished suppressive potency of primary Treg clones from IPEXA384T patients.

Slides:

Advertisements

Similar presentations

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

Advertisements

Clonal bias of CD56−CD16+ NK cell subpopulations.

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

MP cells are generated from naïve cells in the periphery.

Enhancement of Treg suppressive function by allosteric modification of TIP60. Enhancement of Treg suppressive function by allosteric modification of TIP60.

Impaired development of Treg cell function upon overexpression of FOXP3A384T in naïve CD4+CD25− T cells. Impaired development of Treg cell function upon.

Colonic Treg TCRs (CT2 and CT6) drive Teff cell development in inflammation. Colonic Treg TCRs (CT2 and CT6) drive Teff cell development in inflammation.

Therapeutic effects of TIP60 allosteric modification in DSS-induced colitis. Therapeutic effects of TIP60 allosteric modification in DSS-induced colitis.

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

Tfr cells’ transcriptomic profile distinguishes them from Treg and Tfh cells. Tfr cells’ transcriptomic profile distinguishes them from Treg and Tfh cells.

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.

Improvement in the transcriptional activity of FOXP3A384T by enhancement of TIP60-FOXP3 interaction. Improvement in the transcriptional activity of FOXP3A384T.

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

Resistance of CD141+ DCs to influenza virus in vivo in humanized mice.

Virus-specific T cell responses are detected in all MERS survivors.

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.

Target cell lysis by ZnT8186–194-reactive CD8+ T cell clones.

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.

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

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.

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.

Differential expression of TRM markers by donor- and recipient-derived T cells with time. Differential expression of TRM markers by donor- and recipient-derived.

Dectin-1 is repressed in allergic individuals.

Blood Tfr cells are lymphoid tissue–derived Tfr precursors.

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

Blood Tfr cells are indicators of ongoing humoral activity.

MP cells are generated from naïve cells in the periphery.

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.

CD4+CLA+CD103+ T cells constitute a unique cell population in human blood. CD4+CLA+CD103+ T cells constitute a unique cell population in human blood. (A)

MK-8628 suppresses T lymphocyte proliferation.

CD4+CLA+CD103+T cells from human blood and skin share a functional profile. CD4+CLA+CD103+T cells from human blood and skin share a functional profile.

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.

Dynamic regulation of cell metabolism and mTORC1 activity and the requirement of RAPTOR in thymocyte development. Dynamic regulation of cell metabolism.

RORα deficiency in Tregs results in exaggerated skin inflammation in response to EC sensitization. RORα deficiency in Tregs results in exaggerated skin.

CD25 surface expression and TCR signal strength predict T helper differentiation and memory potential of early effector T cells in vivo. CD25 surface expression.

Northern blot analysis of hY4 in CLL-derived exosomes and cells.

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.

Map of sites with ages and postulated early and later pathways associated with modern humans dispersing across Asia during the Late Pleistocene. Map of.

Enhancement of Treg suppressive function by allosteric modification of TIP60. Enhancement of Treg suppressive function by allosteric modification of TIP60.

Human Tfr cells do not express CD25.

Fig. 2 Phenotypic analyses of Bcl11b-deficient Treg cells.

Partial alteration of the Treg gene signature by the p.A384T mutation.

Fig. 2 Regulation of CD73 and CD39 cell membrane expressions and extracellular adenosine levels by ERs in osteoprogenitor cells. Regulation of CD73 and.

Fig. 2 Direct ex vivo cross-recognition analysis of disease-relevant islet-specific T cells. Direct ex vivo cross-recognition analysis of disease-relevant.

CD4+ memory T cells derived from either CD25hi or CD25lo effector cells respond robustly to secondary challenge. CD4+ memory T cells derived from either.

Fig. 3 Regulation of CD73 and CD39 cell membrane expression and extracellular adenosine levels by ERs in osteoclasts. Regulation of CD73 and CD39 cell.

Colonic Treg TCRs react to MA Helicobacter species.

SLC30A8 and INS gene expression in mTECs and circulating islet-reactive CD8+ T cell frequencies in HLA-A2+ and HLA-A2− healthy donors. SLC30A8 and INS.

Treg expression of Gata3 plays a major role in controlling dermal fibrosis. Treg expression of Gata3 plays a major role in controlling dermal fibrosis.

Tregs preferentially regulate TH2 cytokines in skin.

Patient Tregs express normal levels of suppression.

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.

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.

Acute circadian disruption alters ILC3 cytokine secretion.

REV-ERBα deficiency reduces frequency and number of NKp46+ ILC3s.

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.

Fetal-derived γδ T cells infiltrate the meninges from birth.

T cell–derived IL-13 is essential for the inception of AHR.

Bb monocolonization enhances Treg population in the cLP.

CSGG-induced iTreg cells are capable of suppressing intestinal inflammation. CSGG-induced iTreg cells are capable of suppressing intestinal inflammation.

Presentation transcript:

Diminished suppressive potency of primary Treg clones from IPEXA384T patients. Diminished suppressive potency of primary Treg clones from IPEXA384T patients. (A) FOXP3 and CD25 expression in CD4+ cells of IPEXA384T patients and age- and sex-matched controls ex vivo. The FOXP3 MFI levels of CD25+FOXP3+ cells were determined in independent assessments and were normalized to the corresponding healthy controls. (B to E) Pools of single cell–derived clones of FOXP3+ and FOXP3− CD4+ T cells were generated from IPEX patients (shown as IPEX 1 and 2) and their corresponding controls (Control 1 and 2). (B) FOXP3 and CD25 expression at the harvest of the clones. (C) Cytokine production assessed by flow cytometry. (D) Proliferation of individual T cell clones in the absence of exogenous rhIL-2. cpm, counts per minute. (E) Suppression of proliferation of allogeneic CD4+CD25− T cells. Clone sample sizes: IPEX 1: FOXP3+ = 5, FOXP3− = 14; Control 1: FOXP3+ = 17, FOXP3− = 19; IPEX 2: FOXP3+ = 110, FOXP3− = 10, Control 2: FOXP3+ = 70, FOXP3− = 41. Data are presented as individual clones with line at median ± interquartile range. All data sets were compared with one-way nonparametric ANOVA (P < 0.0001) and followed by Dunn’s posttest. Khalid Bin Dhuban et al. Sci. Immunol. 2017;2:eaai9297 Copyright © 2017 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.