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Remission of collagen-induced arthritis by adoptive transfer of peritoneal cells
T. Liu1, L. Chang2, Y.-M. Jiang3
- Department of Laboratory Medicine, West China Second University Hospital, and Key Laboratory of Obstetric & Gynaecologic and Paediatric Diseases and Birth Defects of Ministry of Education, Sichuan University, Chengdu, and State Key Laboratory of Biotherapy and Cancer Center/National Collaborative Innovation Center for Biotherapy, Sichuan University, Chengdu, China.
- Paediatric Diseases and Birth Defects of Ministry of Education, Sichuan University, Chengdu, China.
- Department of Laboratory Medicine, West China Second University Hospital, and Key Laboratory of Obstetric & Gynaecologic and Paediatric Diseases and Birth Defects of Ministry of Education, Sichuan University, Chengdu, China. jiangym_scu@163.com
CER12811
2020 Vol.38, N°6
PI 1161, PF 1169
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PMID: 32141431 [PubMed]
Received: 26/09/2019
Accepted : 20/01/2020
In Press: 05/03/2020
Published: 03/12/2020
Abstract
OBJECTIVES:
The collagen-induced arthritis (CIA) model shares both immunological and pathological features with human rheumatoid arthritis (RA), thus it has been used extensively as a model to study the pathogenesis of RA and for testing therapeutics. It is well-known that the T helper cell 17 (Th17) responses are involved in the pathogenesis of RA, while the regulatory T cells (Tregs) are considered to limit the progress of disease. Previously, we found that peritoneal cells (PCs) possess immunosuppressive characteristics and it is conceivable that PCs potentially have the therapeutic benefits for RA. In this study, we investigated whether PCs are capable of Treg induction and therefore suppress Th17-mediated CIA.
METHODS:
Naïve PCs were intravenously transferred into CIA mice at the early clinical signs of arthritis. The treatment commenced on day 0 and then every other day until day 14. Clinical symptoms of arthritis, histological changes, cytokine expressions and cell population profiles were investigated.
RESULTS:
Intravenously administrating PCs ameliorated the severity of CIA. Further investigations unveiled that the reduction of Th17 cells and the induction of Tregs is ascribed to the remission of the disease. Specifically, when splenic PBMC were cultured with PCs, the expression of FOXP3 and IFN-γ was markedly induced. It is suggested that IFN-γ secreted by PCs plays an important role in the conversion of CD4+T cells to Tregs.
CONCLUSIONS:
The adoptive transfer of PCs is effective in the treatment of CIA by regulating the T cell differentiations. Our findings might provide a new strategy for RA therapy.
