Reciprocal Activation of Fibroblast-like Synoviocyte and Type II Collagen-reactive T cell in Rheumatoid Arthritis.
- Author:
Chong Hyeon YOON
1
;
Mi Kyung PARK
;
Mi La CHO
;
Hyeok Jae KO
;
Kyung Soo PARK
;
Wan Uk KIM
;
Jun Ki MIN
;
Sang Heon LEE
;
Yeon Sik HONG
;
Sung Hwan PARK
;
Chul Soo CHO
;
Ho Youn KIM
Author Information
1. Division of Rheumatology, Department of Internal Medicine, College of Medicine, The Catholic University of Korea.ho@catholic.ac.kr
- Publication Type:Original Article
- Keywords:
Type II collagen;
T cell;
Fibroblast-like synoviocyte;
RA
- MeSH:
Arthritis, Rheumatoid*;
Coculture Techniques;
Collagen Type II;
Cytokines;
Enzyme-Linked Immunosorbent Assay;
Flow Cytometry;
Humans;
Interleukin-15;
Interleukin-17;
T-Lymphocytes;
Tumor Necrosis Factor-alpha
- From:The Journal of the Korean Rheumatism Association
2004;11(1):25-36
- CountryRepublic of Korea
- Language:Korean
-
Abstract:
OBJECTIVE: To investigate the interaction between type II collagen (CII)-reactive T cell and fibroblast-like synoviocyte in rheumatoid arthritis (RA). METHODS: Peripheral blood T cells from RA patients were cultured with bovine CII and analyzed by flow cytometry. After co-culture with CII-reactive T cells and fibroblast-like synoviocytes (FLS), the expression of cytokines (IL-15 and TNF-alpha from FLS, IFN-gamma and IL-17 from CII-reactive T cells) were determined by ELISA and RT-PCR. RESULTS: CII-reactive T cells expressed CD69, one of the early activation markers, and produced significant amount of IFN-gamma, and proliferated. IL-15 and TNF-alpha expression from FLS were significantly elevated when co-culture with CII-reactive T cells and inhibited by physical interruption of cell-to-cell contact or anti-CD40 antibody. IFN-gamma and IL-17 expression from CII-reactive T cells were also significantly elevated when co-culture with FLS and inhibited by anti-IL-15 monoclonal antibody. CONCLUSIONS: CII-reactive T cells can activate FLS to secret proinflammatoy cytokines and interactions between these two cells drive further activation of each other. These data suggest that CII-reactive T cell may play a important role in pathogenesis of RA.
