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Human T cells that are able to produce IL‐17 express the chemokine receptor CCR6
Author(s) -
Singh Satya,
Zhang Hongwei,
Foley John,
Hedrick Michael,
Farber Joshua
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1069.2
Subject(s) - c c chemokine receptor type 6 , chemokine receptor , ccl5 , microbiology and biotechnology , cytotoxic t cell , cd8 , biology , t cell , chemokine , interleukin 21 , immune system , immunology , il 2 receptor , chemistry , in vitro , biochemistry
A new lineage of effector/memory CD4 + T cells has been identified whose signature products are IL‐17 cytokines and whose differentiation requires the nuclear receptor, RORγt. These Th17 cells are critical effectors in mouse models of autoimmune disease. We have analyzed the association between chemokine receptor expression and IL‐17 production for human T cells. Activating cord blood (naïve) CD4 + T cells under conditions driving Th17 differentiation led to preferential induction of CCR6, CCR9 and CXCR6. Despite these data, we found no strong correlation between the production of IL‐17 and expression of CCR9 or CXCR6. By contrast, virtually all IL‐17‐producing CD4 + T cells, either made in our in vitro or found in peripheral blood, expressed CCR6. Compared with CD4 + CD45RO + CCR6 − cells, CD4 + CD45RO + CCR6 + cells contained at least 100‐fold more IL‐17A mRNA and secreted 100‐fold more IL‐17 protein. The CCR6 + cells showed a similar enrichment in mRNA for RORγt. CCR6 was likewise expressed on all IL‐17‐producing CD8 + PBL. CCR6 has been associated with the trafficking of T, B, and dendritic cells to epithelial sites, but has not been linked to a specific T cell phenotype. Our data reveal a fundamental feature of IL‐17‐producing human T cells and a novel role for CCR6, suggesting both new directions for investigating IL‐17‐related immune responses and possible targets for preventing inflammatory injury. Research support: NIAID, NIH