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A distinct CD38+CD45RA+ population of CD4+, CD8+, and double-negative T cells is controlled by FAS

ME. Maccari, S. Fuchs, P. Kury, G. Andrieux, S. Völkl, B. Bengsch, MR. Lorenz, M. Heeg, J. Rohr, S. Jägle, CN. Castro, M. Groß, U. Warthorst, C. König, I. Fuchs, C. Speckmann, J. Thalhammer, FG. Kapp, MG. Seidel, G. Dückers, S. Schönberger, C....

. 2021 ; 218 (2) : . [pub] 20210201

Jazyk angličtina Země Spojené státy americké

Typ dokumentu časopisecké články, práce podpořená grantem

Perzistentní odkaz   https://www.medvik.cz/link/bmc21026130

The identification and characterization of rare immune cell populations in humans can be facilitated by their growth advantage in the context of specific genetic diseases. Here, we use autoimmune lymphoproliferative syndrome to identify a population of FAS-controlled TCRαβ+ T cells. They include CD4+, CD8+, and double-negative T cells and can be defined by a CD38+CD45RA+T-BET- expression pattern. These unconventional T cells are present in healthy individuals, are generated before birth, are enriched in lymphoid tissue, and do not expand during acute viral infection. They are characterized by a unique molecular signature that is unambiguously different from other known T cell differentiation subsets and independent of CD4 or CD8 expression. Functionally, FAS-controlled T cells represent highly proliferative, noncytotoxic T cells with an IL-10 cytokine bias. Mechanistically, regulation of this physiological population is mediated by FAS and CTLA4 signaling, and its survival is enhanced by mTOR and STAT3 signals. Genetic alterations in these pathways result in expansion of FAS-controlled T cells, which can cause significant lymphoproliferative disease.

1st Department of Medicine Division of Infectious Diseases University Medical Center Hamburg Eppendorf Hamburg Germany

Bioinformatics Institute for Computer Science Faculty of Engineering University of Freiburg Germany

Bioss Centre for Biological Signalling Studies University of Freiburg Freiburg Germany

Center for Integrative Biological Signaling Studies Albert Ludwigs University Freiburg Germany

Childhood Leukemia Investigation Prague Department of Pediatric Hematology and Oncology 2nd Medical School Charles University and University Hospital Motol Prague Czech Republic

Department of Biochemistry University of Lausanne Epalinges Switzerland

Department of General Paediatrics Clinic Oldenburg Oldenburg Germany

Department of General Paediatrics Clinic Sankt Augustin Sankt Augustin Germany

Department of Internal Medicine 5 Hematology Oncology University of Erlangen Erlangen Germany

Department of Medicine 2 Gastroenterology Hepatology Endocrinology and Infectious Diseases Medical Center University of Freiburg Faculty of Medicine University of Freiburg Freiburg Germany

Department of Pediatric and Adolescent Medicine University Hospital of Cologne Cologne Germany

Department of Pediatric Hematology and Oncology University Hospital Motol and 2nd Faculty of Medicine Charles University Prague Czech Republic

Department of Pediatric Hematology Oncology University of Duisburg Essen Essen Germany

Department of Pediatric Pulmonology Allergy and Neonatology Hannover Medical School Hannover Germany

Department of Pediatrics Friedrich Alexander University Erlangen Nürnberg Erlangen Germany

Department of Pediatrics University Hospital Carl Gustav Carus Technische Universität Dresden Dresden Germany

Department of Rheumatology and Clinical Immunology Medical Center University of Freiburg Faculty of Medicine University of Freiburg Freiburg Germany

Division of Pediatric Hematology and Oncology Department of Pediatrics and Adolescent Medicine Medical Center University of Freiburg Faculty of Medicine University of Freiburg Freiburg Germany

Division of Pediatric Hematology Oncology Department of Pediatrics and Adolescent Medicine Medical University Graz Graz Austria

Faculty of Biology University of Freiburg Freiburg Germany

German Cancer Consortium Freiburg and German Cancer Research Center Heidelberg Germany

German Center for Infection Research Satellite Center Freiburg Germany

Great North Children's Hospital Newcastle upon Tyne Hospitals NHS Foundation Trust Newcastle upon Tyne UK

Haematology Unit Istituto di Ricovero e Cura a Carattere Scientifico Istituto Giannina Gaslini Genoa Italy

Helios Kliniken Krefeld Children's Hospital Krefeld Germany

Institute for Clinical Transfusion Medicine and Immunogenetics Ulm German Red Cross Blood Service Baden Wuerttemberg Hessen Ulm Germany

Institute for Immunodeficiency Center for Chronic Immunodeficiency Medical Center University of Freiburg Faculty of Medicine University of Freiburg Freiburg Germany

Institute for Transfusion Medicine University of Ulm Ulm Germany

Institute of Health and Society Newcastle University Newcastle upon Tyne UK

Institute of Human Genetics University of Erlangen Erlangen Germany

Institute of Medical Bioinformatics and Systems Medicine Medical Center University of Freiburg Faculty of Medicine University of Freiburg Freiburg Germany

Resolving Infection Susceptibility Cluster of Excellence 2155 Hanover Medical School Satellite Center Freiburg Germany

Roche Pharma Research and Early Development Immunology Infectious Diseases and Ophthalmology Discovery and Translational Area Roche Innovation Center Basel Basel Switzerland

University of Bonn Department of Paediatric Haematology and Oncology University Children's Hospital Bonn Germany

Citace poskytuje Crossref.org

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$a The identification and characterization of rare immune cell populations in humans can be facilitated by their growth advantage in the context of specific genetic diseases. Here, we use autoimmune lymphoproliferative syndrome to identify a population of FAS-controlled TCRαβ+ T cells. They include CD4+, CD8+, and double-negative T cells and can be defined by a CD38+CD45RA+T-BET- expression pattern. These unconventional T cells are present in healthy individuals, are generated before birth, are enriched in lymphoid tissue, and do not expand during acute viral infection. They are characterized by a unique molecular signature that is unambiguously different from other known T cell differentiation subsets and independent of CD4 or CD8 expression. Functionally, FAS-controlled T cells represent highly proliferative, noncytotoxic T cells with an IL-10 cytokine bias. Mechanistically, regulation of this physiological population is mediated by FAS and CTLA4 signaling, and its survival is enhanced by mTOR and STAT3 signals. Genetic alterations in these pathways result in expansion of FAS-controlled T cells, which can cause significant lymphoproliferative disease.
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