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The British Journal of Rheumatology, Vol 37, 1207-1214, Copyright © 1998 by British Society for Rheumatology

ORIGINAL PAPERS

Interleukin-10 inhibits the capacity of synovial macrophages to function as antigen-presenting cells

M Mottonen, P Isomaki, R Saario, P Toivanen, J Punnonen and O Lassila
Turku Immunology Centre, Department of Medical Microbiology, Turku University, Finland.

OBJECTIVE: We have investigated the effects of interleukin (IL)-10, IL- 4 + granulocyte/macrophage colony-stimulating factor (GM-CSF) and tumour necrosis factor alpha (TNF-alpha) on the phenotype and antigen- presenting capacity of synovial fluid (SF) macrophages from patients with rheumatoid arthritis. METHODS: The effects of IL-4, IL-10, GM-CSF and TNF-alpha on the expression of surface antigens on SF macrophages were studied using flow cytometry. The effects of these cytokines on the capacity of SF macrophages to activate T cells was investigated using the allogeneic mixed lymphocyte reaction (MLR). RESULTS: IL-10 reduced the expression of CD40, CD86 and HLA-DR, and increased the expression of CD14, on SF macrophages. IL-10 had no effect on the expression of CD80. Importantly, these effects of IL-10 on the phenotype of SF macrophages appear to have functional consequences, because cells incubated with IL-10 had a significantly reduced capacity to activate T cells in MLR. The effects of IL-4, GM-CSF and TNF-alpha were generally opposite to those observed in response to IL-10. IL-4 + GM-CSF, a combination of cytokines known to induce differentiation of dendritic cells, increased the expression of CD40, CD80 and CD86, and decreased the expression of CD14 on SF macrophages. Accordingly, IL-4 + GM-CSF increased the capacity of SF macrophages to activate T cells in MLR. IL-10 inhibited the effects of IL-4 + GM-CSF on SF macrophages. CONCLUSIONS: IL-10 inhibits the antigen-presenting capacity of SF macrophages, which further emphasizes the anti-inflammatory potential of IL-10 in RA. Importantly, IL-10 is able to downregulate the APC function of SF macrophages even when they are efficiently activated.
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