| Summary: | 碩士 === 國立陽明大學 === 臨床醫學研究所 === 97 === The regulatory T cells (Tregs) exert immunoregulartory function and are critical in maintain self-tolerance. Their roles in seronegative spondyloarthritis (SpA), such as the prototype of SpA-ankylosing spondylitis (AS), have not been clearly defined and well-surveyed. The present investigation is to measure the percentage of Tregs in AS and to delineate their correlation with the serum levels of cytokines, clinical demographic characteristics as well as disease activity index.
We included 69 AS patients (fifteen of them received tumor necrosis factor-α blocker-adalimumab treatment for three months) and used questionnaires to record the demographic data, disease activity index and functional index. Serum levels of cytokines including interlukin-2, 4, 10 (IL-2, 4, 10), tumor necrosis factor-α (TNF-α), interferon-γ (IFN-γ) and transforming growth factor-β (TGF-β) were measured. Erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP) were also determined. Thirty healthy subjects served as control. The peripheral blood mononuclear cells (PBMCs) were stained with anti-CD4, anti-CD25 and anti-FoxP3 antibodies and the flow-cytometry was used to determine cell populations.
The percentages of CD4+CD25+, CD4+CD25+FoxP3+, CD4+CD25-FoxP3+, CD25+FoxP3+ Tregs in PBMCs and serum levels of IL-10, TGF-β, TNF-α were significantly higher in AS patients than in healthy controls, while IL-2, IL-4 and IFN-γ were higher in normal controls (p<0.05). In AS patients with poor functional index, ESR and CRP levels were higher and correlated significantly with Bath Ankylosing Spondylitis Functional Index (BASFI) (r=0.33 and 0.421, p=0.001, respectively). Among AS patients, there were statistically significant correlations between ESR/ CRP level and the frequencies of CD4+CD25+/ CD4+CD25+FoxP3+/ CD4+CD25-FoxP3+/ CD25+FoxP3+ (r=0.35 to 0.43, and p<0.05) in PBMCs. After adalimumab treatment, the percentages of CD4+CD25+ Tregs, ESR/CRP and Bath Ankylosing Spondylitis Disease Activity Index (BASDAI)/ BASFI in 15 patients were significantly and gradually decreased over time (GEE β=-0.11 to -10.18, p=0.025 to <0.001).
In conclusion, the high expression of FoxP3+ and CD25+ on CD4+ T cells in patients with AS was demonstrated and it could be reversed by the anti-TNF-α therapy. The findings have suggested that Tregs may play a role to modulate the inflammatory process in AS. Whether Tregs can be regarded as a predictor for treatment outcome is unclear and requires further study.
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