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Regulation of Th17 differentiation by epidermal fatty acid binding protein, E‐FABP
Author(s) -
LI BING,
REYNOLDS JOSEPH M.,
STOUT ROBERT D.,
SUTTLES JILL
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.1073.20
Subject(s) - proinflammatory cytokine , t cell , biology , microbiology and biotechnology , experimental autoimmune encephalomyelitis , antigen presentation , immunology , chemistry , inflammation , immune system
Fatty acid binding proteins, FABPs, have been identified as central regulators of both metabolic and inflammatory pathways. Mice deficient for expression of E‐FABP display protection from development of experimental autoimmune encephalomyelitis, exhibiting reduced expression of proinflammatory cytokines, including IFNγ and IL‐17, as compared to wild‐type mice. FABP‐deficient macrophages and dendritic cells (DC) are defective in expression of inflammatory cytokines and are inefficient in the promotion of proinflammatory T cells responses during antigen presentation. However, E‐FABP expression by T cells, themselves, was found to influence T cell cytokine expression. Purified naive CD4+ T cells from female wild‐type and E‐FABP‐deficient mice were driven towards a Th17 phenotype by culture with TGFβ and IL‐6. Flow cytometric analysis revealed that wild‐type T cell cultures contained over twice the levels of IL‐17 positive cells than did T cells isolated from E‐FABP‐deficient mice. Interestingly, when these experiments were performed using naive T cells from male mice, no differences in IL‐17 expression were observed. Overall, our studies demonstrate that E‐FABP expression by macrophages and DC promotes Th1 and Th17 differentiation. However, T cell expression of E‐FABP also plays a role in Th17 differentiation, directly, in a gender specific manner.