期刊
NEUROTHERAPEUTICS
卷 4, 期 4, 页码 666-675出版社
SPRINGER
DOI: 10.1016/j.nurt.2007.07.006
关键词
T-cell activation; CD28/B7 molecules; co-stimulation blockade; CT1A-4 ig; EAE/MS; monoclonal antibody (mAb)
资金
- NIAID NIH HHS [AI043496, U19 AI046130, AI058680] Funding Source: Medline
The modulation of co-stimulatory pathways represents a novel therapeutic strategy to regulate autoimmune diseases. Auto-reactive CD4+ T cells play a critical role in initiating the immune response leading to inflammation and autoimmune diseases. Blocking co-stimulatory signals prevents T-cell activation, thus diminishing autoimmune responses and possibly preventing the progression of autoimmune disease. Blockade of several co-stimulatory pathways has been investigated in animal models and has led to clinical trials testing specific blocking agents in humans. In this review we will describe the role of co-stimulatory pathways, primarily the CD28-B7 pathway, in autoimmune diseases, and we will present in vivo and in vitro studies supporting the efficacy of co-stimulation blockade in animal models of autoimmune disease. Finally, we will discuss the clinical therapeutic efficacy of blocking monoclonal antibodies in preventing or reducing autoantigen driven T-cell activation in humans with particular attention to the CD28/B7 pathway. Inhibiting co-stimulatory molecule interactions by using monoclonal antibodies seems to be an original approach to regulate autoimmune diseases in humans. Key Words: T-cell activation, CD28/B7 molecules, co-stimulation blockade, CTIA-4 Ig, EAE/MS, monoclonal antibody (mAb).
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据