Hueber AJ, Asquith DL, Miller AM et al.
J Immunol 2010;184:3336–40.
Interleukin-17A (IL-17A) is a potent pro-inflammatory cytokine that has been implicated in the pathogenesis of rheumatoid arthritis. This group investigated its cellular origin in human synovial specimens and found, surprisingly, that mast cells rather than Th17 T cells appear to represent a major source.
The list of mediators with potential pro-inflammatory relevance in rheumatoid arthritis (RA) grows ever longer, including tumor necrosis factor (TNF), interleukin-1 (IL-1), IL-6, leukotriene B4, and others. IL-17A was the first cytokine of the IL-17 family to be described; it promotes local inflammation by eliciting secretion from fibroblasts and epithelial cells of a range of cytokines and chemokines. The result is a marked amplification effect, such that a limited number of IL-17A producers can effect an impressive recruitment of neutrophils and other inflammatory cells. While multiple hematopoietic lineages are capable of IL-17A secretion, the canonical source is a lineage of CD4+ T helper cells termed Th17 cells. To determine potential sources of IL-17A in rheumatoid synovium, Hueber and colleagues performed immunostaining on RA and osteoarthritis (OA) synovial tissues obtained at joint replacement surgery.