Interleukin-7 is required for CD4+ T cell activation and autoimmune neuroinflammation

Brian R. Lawson, Rosana Gonzalez-Quintial, Theodoros Eleftheriadis, Michael A. Farrar, Stephen D. Miller, Karsten Sauer, Dorian B. McGavern, Dwight H. Kono, Roberto Baccala, Argyrios N. Theofilopoulos

Research output: Contribution to journalArticlepeer-review

27 Scopus citations


IL-7 is known to be vital for T cell homeostasis but has previously been presumed to be dispensable for TCR-induced activation. Here, we show that IL-7 is critical for the initial activation of CD4+ T cells in that it provides some of the necessary early signaling components, such as activated STAT5 and Akt. Accordingly, short-term in vivo IL-7Rα blockade inhibited the activation and expansion of autoantigen-specific CD4+ T cells and, when used to treat experimental autoimmune encephalomyelitis (EAE), prevented and ameliorated disease. Our studies demonstrate that IL-7 signaling is a prerequisite for optimal CD4+ T cell activation and that IL-7R antagonism may be effective in treating CD4+ T cell-mediated neuroinflammation and other autoimmune inflammatory conditions.

Original languageEnglish (US)
Pages (from-to)260-269
Number of pages10
JournalClinical Immunology
Issue number2
StatePublished - Dec 1 2015

Bibliographical note

Publisher Copyright:
© 2015 Elsevier Inc.


  • EAE
  • IL-7
  • Signaling pathways
  • T cells


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