Chemically-Initiated Hyperglycemia: Streptozotocin-Specific T Lymphocyte Reactions
During the past 15 years ample evidence has been accumulated that immunological reactions are involved in the development of insulin-dependent diabetes mellitus, i.e. Type I diabetes. It is currently widely thought that insulin-deficiency results from a chronic, organ-specific autoimmune reaction ultimately resulting in beta-cell destruction. Despite abundant data on both humoral and cellular abnormal immunological patterns detectable during the clinically silent prediabetic period, to date unequivocal demonstration of a direct pernicious autoimmune lesion of the beta-cells is still missing (1). Based on epidemiological investigations, it is noted that environmental factors most likely trigger the disease process in susceptible individuals. In support of such an initiating event are the marked discordance rate of approximately 50% in identical twins (D. Pyke, Chapter 31), the increased frequency of children with Type I diabetes with the congenital rubella syndrome (2), and the enhancing and preventing effect of dietary constituents on the incidence of diabetes in the diabetes-prone BB rat (F.W. Scott, Chapter 34). In all these situations the participation of autoimmune signs is unquestionable, yet the beta-cell specific immunopathogenic pathway still remains to be defined.
KeywordsSpleen Cell Popliteal Lymph Node Congenital Rubella Syndrome Hind Footpad Spleen Cell Donor
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- 2.Ginsberg-Fellner, F., Witt, M.E., Fedun, B., Taub, F., Doberson, M.J., McEvoy, R.C., Cooper, L.Z., Notkins, A.L., Rubinstein, P., 1985, Diabetes mellitus and autoimmunity in patients with congenital rubells syndrome. Rev Infect Dis 7: 170–5 (Suppl 1).Google Scholar