Fibrotic disease and the TH1/TH2 paradigm

被引:1338
作者
Wynn, TA [1 ]
机构
[1] NIAID, Parasit Dis Lab, NIH, Bethesda, MD 20892 USA
关键词
D O I
10.1038/nri1412
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Tissue fibrosis ( scarring) is a leading cause of morbidity and mortality. Current treatments for fibrotic disorders, such as idiopathic pulmonary fibrosis, hepatic fibrosis and systemic sclerosis, target the inflammatory cascade, but they have been widely unsuccessful, largely because the mechanisms that are involved in fibrogenesis are now known to be distinct from those involved in inflammation. Several experimental models have recently been developed to dissect the molecular mechanisms of wound healing and fibrosis. It is hoped that by better understanding the immunological mechanisms that initiate, sustain and suppress the fibrotic process, we will achieve the elusive goal of targeted and effective therapeutics for fibroproliferative diseases.
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收藏
页码:583 / 594
页数:12
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