促炎细胞因子
免疫学
肿瘤坏死因子α
医学
系统性红斑狼疮
自身抗体
细胞因子
自身免疫性疾病
疾病
炎症
抗体
内科学
作者
Martin Aringer,Josef S Smolen
出处
期刊:Arthritis Research
[Springer Nature]
日期:2003-01-01
卷期号:5 (4): 172-172
被引量:110
摘要
Tumor necrosis factor (TNF) is a proinflammatory cytokine and a B-cell growth factor. It has numerous possible effects on T lymphocytes and dendritic cells, and it influences apoptosis. These differential effects may in part explain why patients under TNF-blocker therapy can develop autoantibodies to nuclear antigens, and may shed some light on the finding that low TNF fosters autoimmune disease in some mouse strains. On the contrary, TNF is increased in the blood and in the inflamed kidneys of systemic lupus erythematosus patients. Several studies in lupus-prone mice other than the F1 generation of New Zealand Black mice crossed with New Zealand White mice suggest that TNF is highly proinflammatory in the efferent limb and is potentially detrimental in lupus organ disease. Therefore, TNF blockade probably constitutes an efficacious therapeutic option.
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