期刊
CLINICAL IMMUNOLOGY
卷 102, 期 1, 页码 2-11出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1006/clim.2001.5142
关键词
insulin; insulin peptide B : 9-23; diabetes; autoantibodies; T cells; insulitis; prevention; adoptive transfer; antigen-specific tolerance; mucosal immunity; HLA; altered peptide ligands; peripheral antigen-expressing cells (PAE)
类别
资金
- NCRR NIH HHS [RR 00051, RR 00009] Funding Source: Medline
- NIAID NIH HHS [AI 46374] Funding Source: Medline
- NIDDK NIH HHS [DK 32083, DK 59097, DK 55364] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [U19AI046374] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P01DK055364, R01DK059097, R37DK032083, R01DK032083] Funding Source: NIH RePORTER
At present it is possible to predict the development of type 1A diabetes (immune-mediated diabetes) in man and prevent the disorder in animals. Studies of immunity to insulin play a prominent role in both disease prediction and disease prevention. For both man and the NOD mouse, insulin autoantibodies usually precede the development of diabetes and can be utilized to assist in disease prediction. T cells clones recognizing insulin, both CD4 and CD8, can transfer disease to young mice or immunodeficient animals. Specific insulin peptides reacting with these clones have been identified, their crystal structure when bound to a human diabetogenic MHC allele has been determined, and specific peptides can be used either to induce or to prevent disease. Clinical trials of both insulin and an altered peptide ligand of insulin to prevent islet beta-cell destruction are underway. Insulin is one of a number of islet autoantigens, but it is likely that immune responses to insulin will be central to both pathogenesis and immunologic protection. (C) 2001 Elsevier Science.
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