Background: Rheumatoid arthritis (RA) is a progressive and aggressive autoimmune disease causing swelling, pain, degeneration and loss of function in joints. The pathogenesis of RA has not been fully elucidated. Low-dose Interleukin 2 (IL-2) can promote the proliferation of Treg cells, control inflammatory responses, and maintain immune tolerance in multiple systems, including the joints and the gut.

Objectives: To elucidate the pathogenesis of RA and to explore new effective treatment methods is the focus of current research. In this study, we investigated the effects of low-dose IL-2 on intestinal inflammation in CIA mice.

Methods: We first evaluated joint inflammation in mice. Next, The expression of intestinal inflammatory factors IL-17A and TNF-α, tight junction proteins ZO-1 and Claudin-1, and apoptosis related proteins Bax and Bcl-2 were evaluated.

Results: Compared with the model group, low-dose IL-2 treatment significantly improved walking impairment and reduced joint inflammation in CIA mice. Low-dose IL-2 treatment reduced intestinal inflammation, repaired the intestinal mucosal barrier, and inhibited intestinal epithelial cell apoptosis in CIA mice.

Conclusion: Low-dose IL-2 significantly reduced joint inflammation and intestinal inflammation in CIA mice and is a promising therapeutic modality for the treatment of RA.

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Acknowledgements: NIL.

Disclosure of Interests: None declared.