In vivo activity and in vitro specificity of CD4+ Th1 and Th2 cells derived from the spleens of diabetic NOD mice

CD4+ T cell lines were generated from the spleens of diabetic NOD mice against crude membrane preparations derived from a rat insulinoma. Adoptive transfer of these lines into neonatal mice confirms that overt diabetes is induced by gamma-IFN-secreting Th1 cells, whereas transfer of IL-4-secreting T...

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Bibliographic Details
Published in:The Journal of clinical investigation 1995-06, Vol.95 (6), p.2979-2985
Main Authors: Healey, D, Ozegbe, P, Arden, S, Chandler, P, Hutton, J, Cooke, A
Format: Article
Language:English
Subjects:
AIDS/HIV
Animals
Autoantigens - chemistry
Autoantigens - immunology
CD4-Positive T-Lymphocytes - immunology
Diabetes Mellitus, Type 1 - immunology
Immunity, Cellular
Islets of Langerhans - immunology
Mice
Mice, Inbred NOD - immunology
Molecular Weight
Proteins - chemistry
Proteins - immunology
Spleen - cytology
Th1 Cells - immunology
Th2 Cells - immunology
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Summary:CD4+ T cell lines were generated from the spleens of diabetic NOD mice against crude membrane preparations derived from a rat insulinoma. Adoptive transfer of these lines into neonatal mice confirms that overt diabetes is induced by gamma-IFN-secreting Th1 cells, whereas transfer of IL-4-secreting Th2 cells resulted in a nondestructive peri-islet insulitis. Analysis of the antigens recognized by individual T cell clones from the Th1 line included reactivity against an insulinoma membrane fraction enriched in proteins of approximately 38 kD. Immune responses to the same antigen preparation have been associated with T cell clones derived from human insulin-dependent diabetes mellitus. The specificity of Th2 cells includes reactivity to a fraction enriched in proteins of 30 kD. The data suggest that in insulin-dependent diabetes mellitus the balance between beta cell destruction, associated with intra-islet infiltration, and nondestructive (potential protective) peri-islet insulitis may depend on both the antigens recognized, and the prevailing cytokine environment.
ISSN:0021-9738
DOI:10.1172/jci118006