期刊
JOURNAL OF AUTOIMMUNITY
卷 20, 期 1, 页码 71-81出版社
ACADEMIC PRESS LTD- ELSEVIER SCIENCE LTD
DOI: 10.1016/S0896-8411(02)00106-3
关键词
B7; CD28; CTLA-4; human; multiple sclerosis; myelin
类别
资金
- NIAID NIH HHS [N01AI95380, U01 AI46130, P01 AI39671, P01 AI45757, R01 AI44447] Funding Source: Medline
- NIDDK NIH HHS [R01 DK52127] Funding Source: Medline
- NINDS NIH HHS [R01 NS24247, P01 NS38037] Funding Source: Medline
Multiple sclerosis (MS) is an inflammatory disease of the central nervous system, thought to be mediated in part by an autoimmune response of T cells to protein components of the myelin sheath. The reaction of naive T cells against these antigens requires co-stimulation through CD28. However, the proliferative response of peripheral blood mononuclear cells isolated from patients with MS and stimulated with myelin basic protein (MBP) has been shown to be relatively independent of B7-CD28 co-stimulation, suggesting that dysregulation of co-stimulatory pathways may be involved in the pathogenesis of MS. Here, the role of CTLA-4 engagement was investigated. As expected, blocking CTLA-4-mediated signaling during stimulation of MBP-reactive T cells from healthy controls enhanced the proliferative and cytokine responses. In contrast, CTLA-4 blockade had less effect in patients with MS, suggesting that at least two regulatory mechanisms may be impaired in these individuals. Understanding how co-stimulatory signals may be dysregulated in patients with MS is important at a time when targeting of these pathways is being developed. (C) 2003 Elsevier Science Ltd. All rights reserved.
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