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Protection from autoimmune diabetes by adjuvant therapy non‐obese diabetic mouse: The role of interleukin‐4 and interleukin‐10
Author(s) -
Calcinaro Filippo,
Gambelunghe Giovanni,
Lafferty Kevin J
Publication year - 1997
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1038/icb.1997.72
Subject(s) - insulitis , nod mice , nod , medicine , diabetes mellitus , islet , endocrinology , type 1 diabetes , autoimmune disease , antibody , immunology , cytokine , pancreatic islets , monoclonal antibody , autoimmunity , insulin
Insulin‐dependent diabetes mellitus (IDDM) is an autoimmune disease that is characterized by the destruction of insulin‐producing β‐cells in the pancreatic islets. A single administration of CFA prevents clinical hyperglycaemia in non‐obese diabetic (NOD) mice. We have previously shown that CFA administration does not eliminate insulitis in the pancreas of the treated animals, but diverts the disease process from a destructive to a non‐destructive pathway. We provide evidence that this phenomenon may be under cytokine control. Neutralizing monoclonal antibodies against IL‐4 and IL‐10 were injected, singularly or in combination, into CFA‐treated NOD mice. Antibody treatment did not lead to the development of overt diabetes; however, a marked impairment of glucose tolerance was shown in about one half of the mice treated with a combination of the two antibodies at the end of the study. This functional abnormality correlated with the histological loss of pancreatic islet tissue. These studies suggest a role for IL‐4 and IL‐10 in CFA‐induced protection from diabetes in the NOD mouse. They also suggest that, in this animal model, the nature of the autoimmune response to islet tissue (either destructive or non‐destructive) may reflect the relative proportion of Th1‐ and Th2‐type cytokines produced in the lesions.