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 language | English (US) |
|---|---|
| Pages (from-to) | 260-269 |
| Number of pages | 10 |
| Journal | Clinical Immunology |
| Volume | 161 |
| Issue number | 2 |
| DOIs | |
| State | Published - Dec 1 2015 |
Bibliographical note
Publisher Copyright:© 2015 Elsevier Inc.
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This output contributes to the following UN Sustainable Development Goals (SDGs)
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SDG 3 Good Health and Well-being
Keywords
- EAE
- IL-7
- Signaling pathways
- T cells
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