Maccari, Maria Elena, Fuchs, Sebastian, Kury, Patrick, Andrieux, Geoffroy, Volkl, Simon ORCID: 0000-0003-2193-3048, Bengsch, Bertram ORCID: 0000-0003-2552-740X, Lorenz, Myriam Ricarda, Heeg, Maximilian, Rohr, Jan, Jagle, Sabine, Castro, Carla N., Gross, Miriam, Warthorst, Ursula, Koenig, Christoph, Fuchs, Ilka, Speckmann, Carsten, Thalhammer, Julian ORCID: 0000-0002-0226-1955, Kapp, Friedrich G., Seidel, Markus G., Duckers, Gregor, Schoenberger, Stefan, Schuetz, Catharina, Fuhrer, Marita, Kobbe, Robin, Holzinger, Dirk, Klemann, Christian ORCID: 0000-0002-5639-8690, Smisek, Petr, Owens, Stephen, Horneff, Gerd, Kolb, Reinhard, Naumann-Bartsch, Nora, Miano, Maurizio ORCID: 0000-0002-9816-1704, Staniek, Julian, Rizzi, Marta ORCID: 0000-0002-5153-6089, Kalina, Tomas ORCID: 0000-0003-4475-2872, Schneider, Pascal, Erxleben, Anika, Backofen, Rolf, Ekici, Arif, Niemeyer, Charlotte M., Warnatz, Klaus, Grimbacher, Bodo, Eibel, Hermann, Mackensen, Andreas, Frei, Andreas Philipp, Schwarz, Klaus, Boerries, Melanie, Ehl, Stephan ORCID: 0000-0002-9265-2721 and Rensing-Ehl, Anne (2021). A distinct CD38(+)CD45RA(+) population of CD4(+), CD8(+), and double-negative T cells is controlled by FAS. J. Exp. Med., 218 (2). NEW YORK: ROCKEFELLER UNIV PRESS. ISSN 1540-9538

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Abstract

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 TCR alpha beta(+) 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.

Item Type: Journal Article
Creators:
CreatorsEmailORCIDORCID Put Code
Maccari, Maria ElenaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Fuchs, SebastianUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Kury, PatrickUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Andrieux, GeoffroyUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Volkl, SimonUNSPECIFIEDorcid.org/0000-0003-2193-3048UNSPECIFIED
Bengsch, BertramUNSPECIFIEDorcid.org/0000-0003-2552-740XUNSPECIFIED
Lorenz, Myriam RicardaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Heeg, MaximilianUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Rohr, JanUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Jagle, SabineUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Castro, Carla N.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Gross, MiriamUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Warthorst, UrsulaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Koenig, ChristophUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Fuchs, IlkaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Speckmann, CarstenUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Thalhammer, JulianUNSPECIFIEDorcid.org/0000-0002-0226-1955UNSPECIFIED
Kapp, Friedrich G.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Seidel, Markus G.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Duckers, GregorUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Schoenberger, StefanUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Schuetz, CatharinaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Fuhrer, MaritaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Kobbe, RobinUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Holzinger, DirkUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Klemann, ChristianUNSPECIFIEDorcid.org/0000-0002-5639-8690UNSPECIFIED
Smisek, PetrUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Owens, StephenUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Horneff, GerdUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Kolb, ReinhardUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Naumann-Bartsch, NoraUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Miano, MaurizioUNSPECIFIEDorcid.org/0000-0002-9816-1704UNSPECIFIED
Staniek, JulianUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Rizzi, MartaUNSPECIFIEDorcid.org/0000-0002-5153-6089UNSPECIFIED
Kalina, TomasUNSPECIFIEDorcid.org/0000-0003-4475-2872UNSPECIFIED
Schneider, PascalUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Erxleben, AnikaUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Backofen, RolfUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Ekici, ArifUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Niemeyer, Charlotte M.UNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Warnatz, KlausUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Grimbacher, BodoUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Eibel, HermannUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Mackensen, AndreasUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Frei, Andreas PhilippUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Schwarz, KlausUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Boerries, MelanieUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
Ehl, StephanUNSPECIFIEDorcid.org/0000-0002-9265-2721UNSPECIFIED
Rensing-Ehl, AnneUNSPECIFIEDUNSPECIFIEDUNSPECIFIED
URN: urn:nbn:de:hbz:38-606506
DOI: 10.1084/jem.20192191
Journal or Publication Title: J. Exp. Med.
Volume: 218
Number: 2
Date: 2021
Publisher: ROCKEFELLER UNIV PRESS
Place of Publication: NEW YORK
ISSN: 1540-9538
Language: English
Faculty: Unspecified
Divisions: Unspecified
Subjects: no entry
Uncontrolled Keywords:
KeywordsLanguage
AUTOIMMUNE LYMPHOPROLIFERATIVE SYNDROME; SYNDROME EXPRESS; APOPTOSIS; DEATH; MUTATIONS; EFFECTOR; DIFFERENTIATION; VISUALIZATION; INACTIVATION; ACTIVATIONMultiple languages
Immunology; Medicine, Research & ExperimentalMultiple languages
URI: http://kups.ub.uni-koeln.de/id/eprint/60650

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