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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

Abstract

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
Volume161
Issue number2
DOIs
StatePublished - Dec 1 2015

Bibliographical note

Publisher Copyright:
© 2015 Elsevier Inc.

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

  1. SDG 3 - Good Health and Well-being
    SDG 3 Good Health and Well-being

Keywords

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

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