Publication Date:
1993-02-19
Description:
The T cell receptor (TCR) requirements in the pathogenesis of insulin-dependent diabetes were examined with transgenic NOD mice bearing nondisease-related TCR alpha and beta chains. In both TCR beta and TCR alpha beta transgenic NOD mice the beta chain transgene was expressed by 〉 98% of peripheral T cells. The alpha chain transgene was also highly expressed. Insulitis developed in both sets of transgenic animals with most of the lymphocytes in the lesion expressing the transgenic beta chain and with depletion of the endogenous TCR V beta genes. Nonetheless, NOD animals transgenic for TCR beta and TCR alpha beta developed diabetes similar to controls. Thus, skewing the TCR repertoire did not diminish autoimmune susceptibility in NOD mice.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lipes, M A -- Rosenzweig, A -- Tan, K N -- Tanigawa, G -- Ladd, D -- Seidman, J G -- Eisenbarth, G S -- New York, N.Y. -- Science. 1993 Feb 19;259(5098):1165-9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Joslin Diabetes Center, Harvard Medical School, Brigham and Women's Hospital, Boston, MA 02115.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8267690" target="_blank"〉PubMed〈/a〉
Keywords:
Aging/physiology
;
Animals
;
Base Sequence
;
Crosses, Genetic
;
Diabetes Mellitus, Type 2/genetics/immunology/*physiopathology
;
Female
;
Gene Rearrangement, T-Lymphocyte
;
Islets of Langerhans/immunology/pathology
;
Male
;
Mice
;
Mice, Inbred NOD/*physiology
;
Mice, Transgenic
;
Molecular Sequence Data
;
Oligodeoxyribonucleotides
;
Pancreatic Diseases/genetics/immunology/pathology
;
Polymerase Chain Reaction/methods
;
Receptors, Antigen, T-Cell, alpha-beta/genetics/*physiology
;
T-Lymphocytes/*immunology/pathology
Print ISSN:
0036-8075
Electronic ISSN:
1095-9203
Topics:
Biology
,
Chemistry and Pharmacology
,
Computer Science
,
Medicine
,
Natural Sciences in General
,
Physics
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