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慢性炎症和自身免疫小鼠模型中的TNF病理生理学

TNF pathophysiology in murine models of chronic inflammation and autoimmunity.

作者信息

Kollias George

机构信息

Biomedical Sciences Research Center Al Fleming, Vari, Greece.

出版信息

Semin Arthritis Rheum. 2005 Apr;34(5 Suppl1):3-6. doi: 10.1016/j.semarthrit.2005.01.002.

Abstract

Experimental work in animal models is providing important clues on the specific function of tumor necrosis factor (TNF) and its receptors in disease, especially on the molecular and cellular pathways through which TNF mediates beneficial and deleterious responses. Emerging data on the posttranscriptional regulatory processes, secretion, and postreceptor actions of TNF indicate a variety of mechanisms that may be causative of disease. More recent evidence in murine disease models has indicated heterogeneity of TNF receptor usage in autoimmune disease suppression versus inflammatory tissue damage, suggesting that selective TNF receptor inhibition may be advantageous to anti-TNF treatments in combating chronic inflammatory disease.

摘要

动物模型的实验工作正在为肿瘤坏死因子(TNF)及其受体在疾病中的特定功能提供重要线索,尤其是关于TNF介导有益和有害反应的分子和细胞途径。关于TNF转录后调控过程、分泌及受体后作用的新数据表明,多种机制可能是疾病的病因。小鼠疾病模型的最新证据表明,在自身免疫性疾病抑制与炎症组织损伤中,TNF受体的使用存在异质性,这表明在对抗慢性炎症性疾病时,选择性抑制TNF受体可能比抗TNF治疗更具优势。

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