BIOLOGIC CONTROL OF THE TUMOR-NECROSIS-FACTOR AND INTERLEUKIN-1 SIGNALING CASCADE

被引:38
作者
STEWART, RJ
MARSDEN, PA
机构
[1] UNIV TORONTO, TORONTO, ON M5S 1A8, CANADA
[2] ST MICHAELS HOSP, DIV RENAL, TORONTO, ON M5B 1W8, CANADA
[3] ST MICHAELS HOSP, DEPT MED, TORONTO, ON M5B 1W8, CANADA
基金
英国医学研究理事会;
关键词
CYTOKINE; GLOMERULONEPHRITIS; INFLAMMATION; REJECTION; SEPTIC SHOCK; VASCULITIS;
D O I
10.1016/0272-6386(95)90582-0
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
It is clear that activation of the proinflammatory cytokine cascade is both the cause and the consequence of renal injury, Recently, it has been appreciated that a rich network of signaling pathways contributes to modulation of tumor necrosis factor-alpha (TNF) and interleukin-1 (IL-1) bioactivity, both in vitro and in vivo. Insight into the checks and balances that intervene or temper endogenous cytokine effector mechanisms has arisen from an explosion of new information on the cell biology of proinflammatory cytokines. Novel mechanisms of cytokine regulation are currently being described and hold promise for therapeutic potential: soluble cytokine receptors, endogenous receptor antagonists, and anti-inflammatory cytokines such as IL-4, IL-10, and IL-13. (C) 1995 by the National Kidney Foundation, Inc.
引用
收藏
页码:954 / 966
页数:13
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