Failure of a protective major histocompatibility complex class II molecule to delete autoreactive T cells in autoimmune diabetes
Autor: | William R. Heath, Brett Charlton, Jacques F. A. P. Miller, Robyn M. Slattery |
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Jazyk: | angličtina |
Rok vydání: | 1993 |
Předmět: |
CD4-Positive T-Lymphocytes
Transgene T-Lymphocytes Mice Transgenic Nod Biology medicine.disease_cause Major histocompatibility complex Autoantigens Clonal deletion Autoimmunity Islets of Langerhans Mice Mice Inbred NOD T-Lymphocyte Subsets medicine Animals Cyclophosphamide NOD mice Autoimmune disease Immunity Cellular Multidisciplinary Histocompatibility Antigens Class II Immunization Passive T lymphocyte medicine.disease Diabetes Mellitus Type 1 Immunology biology.protein Female Research Article |
Popis: | The association of major histocompatibility complex genes with autoimmune diseases is firmly established, but the mechanisms by which these genes confer resistance or susceptibility remain controversial. The controversy extends to the nonobese diabetic (NOD) mouse that develops disease similar to human insulin-dependent diabetes mellitus. The transgenic incorporation of certain class II major histocompatibility complex genes protects NOD mice from diabetes, and clonal deletion or functional silencing of autoreactive T cells has been proposed as the mechanism by which these molecules provide protection. We show that neither thymic deletion nor anergy of autoreactive T cells occurs in NOD mice transgenic for I-Ak. Autoreactive T cells are present, functional, and can transfer diabetes to appropriate NOD-recipient mice. |
Databáze: | OpenAIRE |
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