Id2-mediated inhibition of E2A represses memory CD8+ T cell differentiation

Frederick Masson, Martina Minnich, Moshe Olshansky, Ivan Bilic, Adele M. Mount, Axel Kallies, Terence P. Speed, Meinrad Busslinger, Stephen L. Nutt, Gabrielle T. Belz

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54 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)4585-4594
Number of pages10
JournalJournal of Immunology
Issue number9
Publication statusPublished - 1 May 2013
Externally publishedYes

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