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Synovial hyperplasia in HTLV-I associated arthropathy is induced by tumor necrosis factor-α produced by HTLV-I infected CD68+cells
被引:0
作者:
Yin, WH
[1
]
Hasunuma, T
[1
]
Kobata, T
[1
]
Sumida, T
[1
]
Nishioka, K
[1
]
机构:
[1] St Marianna Univ, Sch Med, Inst Med Sci, Rheumatol Immunol & Genet Program,Miyamae Ku, Kawasaki, Kanagawa 2168512, Japan
关键词:
synovial hyperplasia;
HTLV-I;
tumor necrosis factor-alpha;
CD68+cell;
D O I:
暂无
中图分类号:
R5 [内科学];
学科分类号:
1002 ;
100201 ;
摘要:
Objective. To investigate the pathogenic role of macrophage Lineage (CD68+) cells in synovial proliferation in patients with human T cell leukemia virus I (HTLV-I) associated arthropathy (HAAP). Methods. Synovial tissues obtained from 3 patients with HAAP and 3 patients with osteoarthritis (OA) were examined for the expression of tumor necrosis factor-alpha (TNF-alpha) mRNA, HTLV-I tax/rex mRNA, and number of CD68 by in situ reverse transcription assay and immunohistochemistry. Western blot and flow cytometric analyses were used to determine TNF-alpha production in HTLV-I infected synoviocytes. Changes in CD68+ cell population were examined by flow cytometric analysis. Proliferative effects of supernatants of HTLV-I infected synoviocytes on normal synoviocytes were also determined. Results. TNF-alpha and HTLV-I tax/rex mRNA were preferentially expressed in CD68+ cells in HAAP synovia. Infection of OA synoviocytes by HTLV-I resulted in preferential expression in CD68+ cells, and these cells produced TNF-alpha. Supernatants of HTLV-I infected synoviocytes significantly enhanced the proliferation of normal synoviocytes through a TNF-alpha, dependent pathway. Conclusion, Our results suggest HTLV-I viral tropism for CD68+ cells, and that HTLV-I infected synoviocytes were induced to produce TNF-alpha, which enhances synovial proliferation in HAAP.
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页码:874 / 881
页数:8
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