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Investigating the role of the interleukin-23/-17A axis in rheumatoid arthritis
Rheumatology, 10/12/09

Hillyer P et al. – IL-23 is a pro-inflammatory cytokine proposed to be central to the development of autoimmune disease. We investigated whether IL-23, together with the downstream mediator IL-17A, was present and functional in RA in humans. These results suggest that although IL-23 may have pathogenic activity in a proportion of patients with late-stage RA, it is not abundantly produced in this inflammatory tissue, nor does it have a dominant role in all patient tissues analysed.

Methods

RA synovial cells cultured in presence or absence of antibodies directed against IL-23p19 or -23R and -17. IL-23, -12, -17, and their receptors, and IL-6, -1&beta and TNF- measured by ELISA and/or PCR

Results

Small amounts of cell-associated IL-23 (median 110 pg/ml) detected in RA synovial cultures, and found to be functional as IL-23R blockade resulting in significant inhibition of TNF- (57%), IL-1&beta (51%) and IL-6 (30%)
Considerable variability between individual patient samples, and anti-IL-23p19 found to be considerably less effective
IL-17A protein detected in 40% of supernatants and IL-17A blockade, in IL-17A-producing cultures, resulted in small but significant inhibition of TNF- (38%), IL-1&beta (23%) and IL-6 (22%)
Addition of recombinant IL-23 to cultures had variable effect on spontaneous production of endogenous IL-17A with enhancement observed in some but not all cultures

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