Characteristics of Autoimmunity in Type 1 Diabetes and Type 1.5 Overlap With Type 2 Diabetes
- Department of Medicine, and Microbiology and Immunology, Stanford University School of Medicine, Stanford, California
- Address correspondence and reprint requests to Hugh O. McDevitt,Department of Microbiology and Immunology, Stanford University School of Medicine, 299 Campus Dr., D345, Stanford, CA 94305. E-mail: hughmcd{at}stanford.edu
Abstract
This presentation is an overview of mechanisms for developing and maintaining self-tolerance in mammalian organisms. Because this meeting is focused on type 1 diabetes and its mechanisms, the discussion deals primarily with mechanisms of T-cell tolerance, since type 1 diabetes in both effector and initiator phases is primarily a T-cell–mediated autoimmune disease. Emphasis is placed on more recently discovered mechanisms of maintaining self-tolerance (autoimmune regulator [AIRE]) and a new defect in T-cell negative selection. The emerging picture is that of a polygenic disease with various combinations of different alleles of many genes with important roles in the normal immune response or normal immune responses.
- AIRE, autoimmune regulator
- APECED, autoimmune polyendocrinopathy associated with cutaneous abnormalities and ectodermal dysplasia
- IL, interleukin
- MHC, major histocompatibility complex
- TCR, T-cell receptor
Footnotes
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This article is based on a presentation at a symposium. The symposium and the publication of this article were made possible by an unrestricted educational grant from Servier.
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- Accepted May 5, 2005.
- Received March 12, 2005.
- DIABETES
