AB0780 LOW-DOSE IL-2 AMELIORATED PERIPHERAL ARTHRITIS AND INTESTINAL INFLAMMATION IN COLLAGEN-INDUCED ARTHRITIS (CIA) MICE

关节炎 胶原性关节炎 炎症 外围设备 医学 外周血 免疫学 内科学
作者
Chenhui Wang,Cheng Liu
出处
期刊:Annals of the Rheumatic Diseases [BMJ]
卷期号:: 1682.1-1682
标识
DOI:10.1136/annrheumdis-2024-eular.4835
摘要

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.

REFERENCES:

[1] Möller B.; Kollert F.; Sculean A.Villiger P. M. Infectious Triggers in Periodontitis and the Gut in Rheumatoid Arthritis (RA): A Complex Story About Association and Causality. Front Immunol. 2020; 11, 1108. [2] Chahal S.; Biln N.Clarke B. Patient Perspectives on a Digital Mobile Health Application for RA. Open Access Rheumatol. 2021; 13, 63-71. [3] Croia C.; Bursi R.; Sutera D.; Petrelli F.; Alunno A.Puxeddu I. One year in review 2019: pathogenesis of rheu-matoid arthritis. Clin Exp Rheumatol. 2019; 37, 347-357. [4] McDermott G.; Gill R.; Gagne S.; Byrne S.; Huang W.; Wang X.; Prisco L. C.; Zaccardelli A.; Martin L. W.; Masto L.; Kronzer V. L.; Shadick N.; Dellaripa P. F.; Doyle T. J.Sparks J. A. Demographic, Lifestyle, and Serologic Risk Factors for Rheumatoid Arthritis (RA)-associated Bronchiectasis: Role of RA-related Autoantibodies. J Rheumatol. 2022; 49, 672-679. [5] Klatzmann D.Abbas A. K. The promise of low-dose interleukin-2 therapy for autoimmune and inflammatory diseases. Nat Rev Immunol. 2015; 15, 283-294. [6] Wu Y.; Tian Z.Wei H. Developmental and Functional Control of Natural Killer Cells by Cytokines. Front Immunol. 2017; 8, 930.

Acknowledgements:

NIL.

Disclosure of Interests:

None declared.

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