There are much less data on IL-10 in AS compared to ReA. In AS peripheral arthritis is less common than in ReA resulting in less access to synovial fluid and/or synovial membrane. As a consequence, all available data on IL-10 in AS are from peripheral blood. Before better data will be available from the site of inflammation no clear conclusions can yet be drawn.
In one study a correlation between IL-10 levels in plasma and disease activity was reported16 while in another study no difference in median levels of IL10 between AS and controls could be observed.19
To address this question we measured cytokine-positive CD4+ and CD8+ T cells derived from peripheral blood after mitogenic in vitro stimulation by flow cytometry in 25 HLA-B27-positive patients with active AS in comparison to 18 healthy HLA-B27 positive controls and 22 healthy HLA-B27 negative controls.17 AS patients had a significantly lower percentage of IFNy- or TNFa-positive CD4+ T cells compared to HLA-B27-negative controls while the results for HLA-B27-positive healthy control group was in between these 2 groups. For IL-10-positive T cells, we found a significant increase in the CD8+ T cell subpopulation compared to the B27-positive and B27-negative controls (Fig. 3), but not in the CD4+ subpopulation. Thus, there is also a tendency in AS, similar to ReA, to find a higher amount of IL-10 produced by immunocompetent cells compared to controls. A more recent paper looked for IL-10 polymorphism in AS. No significant effect on susceptibility to AS but a possibly minor role in determining age of disease onset and disease activity was found.18
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