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Mast cells are the main IL-17 producing cells in synovium of anti-citrullinated protein antibody-positive and -negative rheumatoid arthritis and osteoarthritis patients
  1. J Suurmond1,
  2. A L Dorjée1,
  3. M R Boon1,
  4. E F Knol2,
  5. T W J Huizinga1,
  6. R E M Toes1,
  7. A J M Schuerwegh1
  1. 1Department of Rheumatology, Leiden University Medical Center, Leiden, The Netherlands
  2. 2Department of Dermatology/Allergology, University Medical Center Utrecht, Utrecht, The Netherlands

Abstract

Background and objectives Recently, evidence is raised that rheumatoid arthritis (RA) can be divided in two main syndromes on the basis of the presence of anti-citrullinated protein antibodies (ACPA). Mast cells have been implicated to play a functional role in mouse models of arthritis as well as human RA, especially in autoantibody-positive disease. Interleukin 17 (IL-17) has also been implicated to play an important role in RA. Recent data in 10 RA patients indicate that mast cells are the main producers of IL-17 in synovial tissue, whereas T cells have also been implicated as a prominent IL-17 producing subset. Therefore, the authors aimed to identify whether expression of IL-17 by mast cells and T cells in synovium is different in ACPA+ and ACPA− RA and osteoarthritis (OA) patients.

Materials and methods Synovial tissue of ACPA+ (n=25) and ACPA− (n=34) RA and OA (n=29) patients was stained for IL-17 in combination with CD117 (mast cells), CD3 (T cells) and CD68 (macrophages) or isotype controls. Concentrations of IL-17 in synovial fluid of ACPA+ (n=30) and ACPA− (n=29) RA and OA (n=14) patients were determined by ELISA.

Results The number of IL-17+ cells was comparable in ACPA+ RA, ACPA− RA and OA patients. The vast majority of IL-17+ cells were mast cells in all three groups (median ranged from 93% to 97%), whereas T cells and macrophages contributed only slightly. Importantly, levels of IL-17 in synovial fluid of ACPA+ RA patients were significantly higher than in ACPA− RA or OA patients.

Conclusions Mast cells are the main cell population producing IL-17 in all three disorders analysed. Possibly, selective activation of mast cells in ACPA+ RA patients is responsible for the increased IL-17 levels in this group. These data are relevant for studies aiming to inhibit IL-17 production in the treatment of arthritis.

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