Journal
IMMUNITY
Volume 41, Issue 2, Pages 230-243Publisher
CELL PRESS
DOI: 10.1016/j.immuni.2014.06.018
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Funding
- Deutsche Forschungsgemeinschaft [SFB992, AR732/1-1, TA436/2-1, TA436/3-1]
- German Federal Ministry of Education and Research, BMBF [01 EO 0803]
- SNF [310030B_133131/1]
- EU
- ERC
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CD8 alpha alpha(+) intraepithelial lymphocytes (IELs) are instrumental in maintaining the epithelial barrier in the intestine. Similar to natural killer cells and other innate lymphoid cells, CD8 alpha alpha(+) IELs constitutively express the T-box transcription factor T-bet. However, the precise role of T-bet for the differentiation or function of IELs is unknown. Here we show that mice genetically deficient for T-bet lacked both TCR alpha beta(+) and TCR gamma delta(+) CD8 alpha alpha(+) IELs and thus are more susceptible to chemically induced colitis. Although T-bet was induced in thymic IEL precursors (IELPs) as a result of agonist selection and interleukin-15 (IL-15) receptor signaling, it was dispensable for the generation of IELPs. Subsequently, T-bet was required for the IL-15-dependent activation, differentiation, and expansion of IELPs in the periphery. Our study reveals a function of T-bet as a central transcriptional regulator linking agonist selection and IL-15 signaling with the emergence of CD8 alpha alpha(+) IELs.
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