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FOXP3 protects conventional human T cells from premature restimulation-induced cell death

Cellular & Molecular Immunology 2021年第1期18卷 194-205页

作者： Kelsey Voss Camille Lake Christopher R.Luthers Nathaniel M.Lott batsukh dorjbal Swadhinya Arjunaraja Bradly M.Bauman Anthony R.Soltis Gauthaman Sukumar Clifton LDalgard Andrew L.Snow Department of Pharmacology&Molecular Therapeutics Uniformed Services University of the Health SciencesBethesdaMD 20817USA The American Genome Center(TAGC) Collaborative Health Initiative Research ProgramUniformed Services University of the Health SciencesBethesdaMDUSA Department of Anatomy Physiology&GeneticsUniformed Services University of the Health SciencesBethesdaMDUSA

The adaptive immune response relies on specific apoptotic programs to maintain homeostasis.Conventional effector T cell(Tcon)expansion is constrained by both forkhead box P3(FOXP3)^(+)-regulatory T cells(Tregs)and restimulation-induced cell death(RICD),a proprlocidal apoptosis pathway triggered by repeated stimulation through the T-cell receptor(TCR).Constitutive FOXP3 expression protects Tregs from RICD by suppressing SLAM-associated protein(SAP),a key adaptor protein that amplifies TCR signaling strength.The role of transient FOXP3 induction in activated human CD4 and CD8 Tcons remains unresolved,but its expression is inversely correlated with acquired RICD sensitivity.Here,we describe a novel role for FOXP3 In protecting human Tcons from premature RICD during expansion.Unlike FOXP3-mediated protection from RICD in Tregs,FOXP3 protects Tcons through a distinct mechanism requiring de novo transcription that does not require SAP suppression.Transcriptome profiling and functional analyses of expanding Tcons revealed that FOXP3 enhances expression of the SLAM family receptor CD48,which in turn sustains basal autophagy and suppresses pro-apoptotic p53 signaling.Both CD48 and FOXP3 expression reduced p53 accumulation upon TCR restimulation.Furthermore,silencing FOXP3 expression or blocking CD48 decreased the mitochondrial membrane potential in expanding Tcons with a concomitant reduction in basal autophagy.Our findings suggest that FOXP3 governs a distinct transcriptional program in early-stage effector Tcons that maintains RICD resistance via CD48-dependent protective autophagy and p53 suppression.

关键词： conventional T cells RICD FOXP3 autophagy CD48

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Nat Genet:单基因突变导致过敏性皮炎的发生

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现代生物医学进展 2017年第27期17卷 I0004-I0004页

作者： Chi A Ma, Yuan Zhang, Michael A Weinreich, Jonathan J Lyons, Celeste G Nelson, Thomas DiMaggio, Kelly D Stone, Joshua D Milner Jeffrey R Stinson, Elisa Ruffo, batsukh dorjbal, Swadhinya Arjunaraja, Kelsey Voss, Andrew L Snow Jordan K Abbott, Pia J Hauk, Paul R Reynolds, Erwin W Gelfand Elisa Ruffo Salomé Glauzy, Natsuko Yamakawa, Eric Meffre Jennifer Stoddard, Julie Niemela, Sergio D Rosenzweig Yu Zhang, Helen F Matthews Joshua J McElwee Nina Jones Alejandro Palma, Matías Oleastro, Emma Prieto, Andrea R Bernasconi, Geronimo Dubra, Silvia Danielian, Jonathan Zaiat, Marcelo A Marti Brian Kim Megan A Cooper Neil Romberg Laboratory of Allergic Diseases National Institute of Allergy and Infectious Diseases National Institutes of Health Bethesda Maryland USA Department of Pharmacology and Molecular Therapeutics Uniformed Services University of the Health Sciences Bethesda Maryland USA Immunodeficiency Diagnosis and Treatment Program Department of Pediatrics National Jewish Health Denver Colorado USA Department of Translational Medicine University of Piemonte Orientale Novara Italy Department of Immunobiology Yale University School of Medicine New Haven Connecticut USA Immunology Service Department of Laboratory Medicine NIH Clinical Center National Institutes of Health Bethesda Maryland USA Human Immunological Disease Section National Institute of Allergy and Infectious Diseases National Institutes of Health Bethesda Maryland USA Merck Research Laboratories Merck and Co. Inc. Boston Massachusetts USA Clinical Research Directorate/Clinical Monitoring Research Program Leidos Biomedical Research Inc. NCI Campus at Frederick Frederick Maryland USA Servicio de Immunología y Reumatología Hospital Nacional de Pediatría Prof. Dr. Juan P. Garrahan Buenos Aires Argentina Division of Dermatology Department of Medicine Washington University School of Medicine St. Louis Missouri USA Department of Pediatrics Division of Rheumatology and Department of Pathology and Immunology Washington University School of Medicine St. Louis Missouri USA Department of Pediatrics Children’s Hospital of Philadelphia Philadelphia Pennsylvania USA.

最近，研究者们鉴定出了一类导致神经性皮炎发生的关键基因突变：CARDll。来自美国NIH过敏与传染病研究所的研究者们通过对四个没有血缘关系的患病家庭进行分析，发现了这一导致疾病产生的基因、

关键词：过敏性皮炎基因突变 Nat 神经性皮炎血缘关系研究所传染病 NIH

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