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American Association of Immunologists, The Journal of Immunology, 9(190), p. 4585-4594, 2013

DOI: 10.4049/jimmunol.1300099

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Id2-Mediated Inhibition of E2A Represses Memory CD8+ T Cell Differentiation

Journal article published in 2013 by Frederick Masson, Martina Minnich, Moshe Olshansky ORCID, Ivan Bilic, Adele M. Mount, Axel Kallies, Terence P. Speed, Meinrad Busslinger, Stephen L. Nutt ORCID, Gabrielle T. Belz ORCID
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

Abstract The transcription factor inhibitor of DNA binding (Id)2 modulates T cell fate decisions, but the molecular mechanism underpinning this regulation is unclear. In this study we show that loss of Id2 cripples effector differentiation and instead programs CD8+ T cells to adopt a memory fate with increased Eomesodermin and Tcf7 expression. We demonstrate that Id2 restrains CD8+ T cell memory differentiation by inhibiting E2A-mediated direct activation of Tcf7 and that Id2 expression level mirrors T cell memory recall capacity. As a result of the defective effector differentiation, Id2-deficient CD8+ T cells fail to induce sufficient Tbx21 expression to generate short-lived effector CD8+ T cells. Our findings reveal that the Id2/E2A axis orchestrates T cell differentiation through the induction or repression of downstream transcription factors essential for effector and memory T cell differentiation.