G-CSF and GM-CSF as therapeutic targets in rheumatoid arthritis

被引：140
|
作者：
Cornish, Ann L. [1 ]
Campbell, Ian K. [2 ]
McKenzie, Brent S. [2 ]
Chatfield, Simon [1 ]
Wicks, Ian P. [1 ]
机构：
[1] Walter & Eliza Hall Inst Med Res, Autoimmun & Transplantat Div, Parkville, Vic 3052, Australia
[2] Bio21 Inst, CSL, Parkville, Vic, Australia
来源：
NATURE REVIEWS RHEUMATOLOGY | 2009年 / 5卷 / 10期
基金：
英国医学研究理事会; 澳大利亚国家健康与医学研究理事会;
关键词：
COLONY-STIMULATING FACTOR; PULMONARY ALVEOLAR PROTEINOSIS; BLOOD NEUTROPHIL COUNTS; INFLAMMATORY ARTHRITIS; DEFICIENT MICE; APOPTOTIC NEUTROPHILS; ANTIRHEUMATIC DRUGS; OPPOSING ACTIONS; SYNOVIAL-FLUID; EFFECTOR PHASE;
D O I：
10.1038/nrrheum.2009.178
中图分类号：
R5 [内科学];
学科分类号：
1002 ; 100201 ;
摘要：
Granulocyte colony-stimulating factor (G-CSF) and granulocyte-macrophage colony-stimulating factor (GM-CSF) are well-recognized regulators of hematopoiesis and have an established role as growth factors in clinical practice. G-CSF and GM-CSF regulate myeloid cell production, differentiation and activation, and might also be important for driving inflammatory responses. Inappropriate engagement of this pathway could be a critical amplification mechanism when maladaptive immune responses predispose to autoimmunity and sterile tissue inflammation. We postulate that antagonism of G-CSF or GM-CSF could represent a novel therapeutic approach for a variety of autoimmune-mediated inflammatory diseases, including rheumatoid arthritis.
引用
收藏
页码：554 / 559
页数：6
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