期刊
JOURNAL OF AUTOIMMUNITY
卷 18, 期 2, 页码 83-94出版社
ACADEMIC PRESS LTD ELSEVIER SCIENCE LTD
DOI: 10.1006/jaut.2001.0573
关键词
autoimmunity; co-stimulatory molecules; EAE/MS; immunotherapy; neuroimmunology
类别
资金
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [T32AI007476] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF NEUROLOGICAL DISORDERS AND STROKE [R01NS034819] Funding Source: NIH RePORTER
- NIAID NIH HHS [AI-07476] Funding Source: Medline
- NINDS NIH HHS [NS34819] Funding Source: Medline
CD28 provides a co-stimulatory signal critical for optimal T cell activation. We and others have shown that the B7/CD28 co-stimulatory pathway is a major regulatory pathway for the control of immune responses. Experimentally induced models of autoimmunity have been shown to be prevented of reduced in intensity in mice deficient for CD28. Here, we show that EAE and accompanying neuroantigen-specific immune responses are drastically reduced in the absence of CD28. However, we go on to show that EAE can be induced in CD28-deficient mice following two immunizations. After re-immunization, CD28-deficient mice develop severe EAE with myelin-specific responses equal to those of wildtype controls, and extensive demyelination in the spinal cord. Treatment of CD28-deficient mice with anti-CD46L at the time of immunization significantly reduced DTH responses and prevented the development of EAE following two immunizations, indicating a critical 0 role for CD40/CD40L signaling in the absence of CD28. Taken together, our results indicate that CD28-mediated co-stimulation does not regulate immunological anergy, Instead, CD28 appears to adjust the threshold for activation and expansion of autoreactive cells. (C) 2002 Elsevier Science Ltd.
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