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

12 Scopus citations

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

Funding Information:
This is manuscript number 29180 from the Department of Immunology and Microbial Science of The Scripps Research Institute. We would like to thank M. Kat Occhipinti for editorial assistance, and John Scatizzi, Dilki Wichramarachchi, and Tannaz Hasnat for excellent technical assistance. This work was supported by grant AR065919 from the NIH National Institute of Arthritis and Musculoskeletal and Skin Diseases .

Keywords

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

Fingerprint Dive into the research topics of 'Interleukin-7 is required for CD4<sup>+</sup> T cell activation and autoimmune neuroinflammation'. Together they form a unique fingerprint.

Cite this