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DOI 10.55563/clinexprheumatol/lnn76t

Медицинская библиотека · Clinical and experimental rheumatology · 2020

Low-dose IL-2 effectively restored decreased regulatory T cells in patients with Behçet's disease.

Liu Xiaoqing, Li Wei, Liu Xiaojie, Luo Jing, Gao Chong, Li Xiaofeng

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Аннотация

OBJECTIVES

Although Behçet's disease (BD) is associated with immune mechanisms, the changes in circulating lymphocytes, especially regulatory T (Treg) cells remain unclear. Furthermore, low dose IL-2 has been reported to promote the expansion of Treg cells. This study aimed to investigate the significance of these subsets in the pathogenesis and the effect of low dose IL-2 on BD.

METHODS

Lymphocyte subsets and cytokines from 177 BD patients and 160 healthy controls (HCs) were characterised. Then the efficacy and safety of low dose IL-2 for refractory BD patients were explored.

RESULTS

There was a decrease in the absolute number of Treg cells and IL-10 in patients, while no difference in Th1, Th2, Th17 cells or their related cytokines. Accordingly, the ratio of Th17/Treg cells in patients was greatly higher than those of healthy controls. Furthermore, circulating Treg levels were negatively correlated with erythrocyte sedimentation rate (ESR), C-reactive protein (CRP) and Behçet's disease current activity form (BDCAF), respectively. Lastly, after IL-2 treatment, all subsets were increased to some degree, while only Treg cells were amplified more dramatically, with a four-fold increase. Meanwhile, we found that the symptoms were mitigated without observed side effects.

CONCLUSIONS

BD might be triggered by the defect of immunotolerance with decreased Treg. Moreover, low-dose IL-2 proposes a potential treatment by restoring Treg and promoting rapidly remission.

Для цитирования: Liu Xiaoqing, Li Wei, Liu Xiaojie, Luo Jing, Gao Chong, Li Xiaofeng. Low-dose IL-2 effectively restored decreased regulatory T cells in patients with Behçet's disease.. Clinical and experimental rheumatology. 2020. DOI: 10.55563/clinexprheumatol/lnn76t.

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