Tissue adaptation of regulatory and intraepithelial CD4 + T cells controls gut inflammation | Zendy

Tomohisa Sujino | Zendy; Mariya London | Zendy; David P. Hoytema van Konijnenburg | Zendy; Tomiko K. Rendon | Zendy; Thorsten Buch | Zendy; Hernandez M. Silva | Zendy; Juan J. Lafaille | Zendy; Bernardo Sgarbi Reis | Zendy; Daniel Mucida | Zendy

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Tissue adaptation of regulatory and intraepithelial CD4 ⁺ T cells controls gut inflammation

Author(s) -

Tomohisa Sujino,

Mariya London,

David P. Hoytema van Konijnenburg,

Tomiko K. Rendon,

Thorsten Buch,

Hernandez M. Silva,

Juan J. Lafaille,

Bernardo Sgarbi Reis,

Daniel Mucida

Publication year - 2016

Publication title -

science

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 12.556

H-Index - 1186

eISSN - 1095-9203

pISSN - 0036-8075

DOI - 10.1126/science.aaf3892

Subject(s) - intraepithelial lymphocyte , lamina propria , foxp3 , inflammation , biology , immunology , intestinal epithelium , microbiology and biotechnology , epithelium , mucosal immunology , limiting , antigen , immune system , immunity , genetics , mechanical engineering , engineering

Foxp3(+) regulatory T cells in peripheral tissues (pT(regs)) are instrumental in limiting inflammatory responses to nonself antigens. Within the intestine, pT(regs) are located primarily in the lamina propria, whereas intraepithelial CD4(+) T cells (CD4(IELs)), which also exhibit anti-inflammatory properties and depend on similar environmental cues, reside in the epithelium. Using intravital microscopy, we show distinct cell dynamics of intestinal T(regs) and CD4(IELs) Upon migration to the epithelium, T(regs) lose Foxp3 and convert to CD4(IELs) in a microbiota-dependent manner, an effect attributed to the loss of the transcription factor ThPOK. Finally, we demonstrate that pT(regs) and CD4(IELs) perform complementary roles in the regulation of intestinal inflammation. These results reveal intratissue specialization of anti-inflammatory T cells shaped by discrete niches of the intestine.

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