Journal
JOURNAL OF IMMUNOLOGY
Volume 184, Issue 7, Pages 3336-3340Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.0903566
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Funding
- Medical Research Council U.K.
- Deutsche Forschungsgemeinschaft
- British Heart Foundation Intermediate Basic Science Research Fellowship [FS/08/035/25309]
- British Heart Foundation [FS/08/035/25309] Funding Source: researchfish
- Medical Research Council [G0700794] Funding Source: researchfish
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The proinflammatory cytokine IL-17A is considered a crucial player in rheumatoid arthritis (RA) pathogenesis. In experimental models of autoimmune arthritis, it has been suggested that the cellular source of IL-17A is CD4(+) T cells (Th17 cells). However, little is known about the source of IL-17 in human inflamed RA tissue. We explored the cellular sources of IL-17A in human RA synovium. Surprisingly, only a small proportion of IL-17-expressing cells were T cells, and these were CCR6 negative. Unexpectedly, the majority of IL-17A expression colocalized within mast cells. Furthermore, we demonstrated in vitro that mast cells produced RORC-dependent IL-17A upon stimulation with TNF-alpha, IgG complexes, C5a, and LPS. These data a-re consistent with a crucial role for IL-17A in RA pathogenesis but suggest that in addition to T cells innate immune pathways particularly mediated via mast cells may be an important component of the effector IL-17A response. The Journal of Immunology, 2010, 184: 3336-3340.
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