Figure 1.

Reduced Candida albicans-induced Th17/IL-17A responses in rheumatoid arthritis. Rheumatoid arthritis (RA) subjects exhibit impaired Candida albicans-specific T-cell responses compared with healthy controls. (A) Peripheral blood mononuclear cells (PBMCs) from RA subjects and controls were cultured for 5 days in media ± heat-killed (HK) C. albicans extract or T-helper type (Th)17 differentiating cytokines (interleukin (IL)-1β, IL-6, IL-23, anti-IL4 and anti-interferon gamma (anti-IFNγ)). IL-17A in cell free culture supernatants was measured by enzyme-linked immunosorbent assay (Student’s t test). (B) Tumor necrosis factor (TNF) alpha inhibitors do not exacerbate C. albicans-specific T-cell responses compared with disease-modifying anti-rheumatic drugs (DMARDs). PBMCs were cultured as in (A) with media alone, HK C. albicans extract or Th17 differentiating cytokines. IL-17A production was assessed in the indicated patient subgroups based on medication use (Mann–Whitney U test). (C) TNFα inhibitors do not alter the fraction of circulating Th17 or Th1 cells in RA subjects with controlled disease. PBMCs from RA subjects and healthy controls were gated on CD3+CD4+ lymphocytes and were analyzed for expression of IL-17A (Th17) and IFNγ+ (Th1) cells. Data were stratified by medication use (Mann–Whitney U test).

Bishu et al. Arthritis Research & Therapy 2014 16:R50   doi:10.1186/ar4480
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