Virus infection islet cell antibodies and islet cell function in type I diabetes mellitus.
The detection of islet cell antibodies has led to an increasing interest in autoimmune mechanisms in Type I diabetes mellitus. Other phenomena, such as insulitis in juvenile diabetics and in experimental animals, cellular immune reactions and concommitant antibodies against other endocrine organs, antinuclear antibodies and circulating immune complexes have supported such speculations. HLA-association and viral-infections could be predisposing and inducing factors. However, with one exception, the occurrence of ICA in a group of mumps infected children did not result in the development of diabetes mellitus over 3-4 years, nor could it be correlated with HLA-pattern. The islet cell antibodies block glucose stimulated insulin secretion in vitro without complement, while Type I diabetic sera with complement are beta cell cytotoxic irrespective of their ICA concentration. It is still not clear whether these mechanisms play any role in vivo. Therapeutic intervention before the clinical manifestation of the disease is as yet not possible due to the lack of markers indicating a subclinical autoimmune process.
D000293:Adolescent; D000328:Adult; D000906:Antibodies; D001323:Autoantibodies; D002648:Child; D002675:Child, Preschool; D003165:Complement System Proteins; D003593:Cytoplasm / Q000276:immunology; D003602:Cytotoxicity, Immunologic; D003922:Diabetes Mellitus, Type 1 / Q000209:etiology*; D006801:Humans; D066298:In Vitro Techniques; D007223:Infant; D007231:Infant, Newborn; D007328:Insulin / Q000378:metabolism; D000078790:Insulin Secretion; D007515:Islets of Langerhans / Q000276:immunology* / Q000378:metabolism; D014777:Virus Diseases / Q000150:complications*
D000906:Antibodies; D001323:Autoantibodies; D007328:Insulin; C024211:islet cell antibody; D003165:Complement System Proteins