Horiuchi Takahiko, Morita Chika, Tsukamoto Hiroshi, Mitoma Hiroki, Sawabe Takuya, Harashima Shin-ichi, Kashiwagi Yoichiro, Okamura Seiichi
Department of Medicine and Biosystemic Science, Kyushu University Graduate School of Medical Sciences, Fukuoka 812-8582, Japan.
Int J Mol Med. 2006 May;17(5):875-9.
Membrane TNF-alpha is a precursor form of soluble TNF-alpha and exerts pro-inflammatory functions in a cell-to-cell contact manner. We showed that membrane TNF-alpha is induced upon activation on the cell surface of CD4+ T cells and CD8+ T cells. In patients with systemic lupus erythematosus (SLE), the percentage of membrane TNF-alpha-bearing CD8+ T cells (41.5+/-12.3%) was significantly higher compared with those of healthy controls (26.7+/-3.9%) (p=0.007) or patients with rheumatoid arthritis (29.8+/-15.4%) (p=0.038). Membrane TNF-alpha-bearing CD8+ T cells from SLE patients displayed cytotoxic activity against L929 cells. It is possible that membrane TNF-alpha may be involved in the increased apoptosis and the generation of autoantigens in SLE.
膜肿瘤坏死因子-α（membrane TNF-alpha）是可溶性肿瘤坏死因子-α的前体形式，以细胞间接触的方式发挥促炎功能。我们发现，膜肿瘤坏死因子-α在CD4+ T细胞和CD8+ T细胞的细胞表面激活后被诱导产生。在系统性红斑狼疮（SLE）患者中，携带膜肿瘤坏死因子-α的CD8+ T细胞百分比（41.5±12.3%）显著高于健康对照组（26.7±3.9%）（p = 0.007）或类风湿性关节炎患者（29.8±15.4%）（p = 0.038）。来自SLE患者的携带膜肿瘤坏死因子-α的CD8+ T细胞对L929细胞表现出细胞毒性活性。膜肿瘤坏死因子-α可能参与了SLE中细胞凋亡增加和自身抗原的产生。
