A longitudinal study of insulin antibodies and anti-insulin cytotoxicity in type I diabetes mellitus
- 22 Downloads
Insulin antibodies and T-cell lymphocyte cytotoxic reactivity against insulin and its related peptides were studied longitudinally in 3 groups of patients with type I diabetes mellitus (DM). Group 1 patients were those in whom the diagnosis was made within 1 week of the initiation diagnosis. They were subdivided into those receiving MC porcine (A) or MC bovine (B) insulin. Group 2 patients were those with a duration of DM for 2–6 years who were receiving either MC porcine (A) or MC bovine (B) insulins. Group 3 subjects were those who had been on conventional recrystallized insulin and then switched to MC porcine (A) or MC bovine (B) insulins for 2 weeks before the start of the study. The incidence of cytotoxic reactions and insulin antibodies were approximately 40–50% for group 1 (either 1A or 1B) at the initiation of the study. At 3-month follow up all patients in group 1B developed insulin antibodies (p<0.02) and a significant increase in the frequency of cytotoxic reactions (p<0.01). By contrast there was a decline in the frequency of cytotoxic reactions in group 1A (p<0.01 at 1 year) and the increase in insulin antibodies was non-significant. Group 2B had higher frequency in cytotoxic reactions (p<0.005) and of insulin antibodies (p<0.05) than group 2A. A significant decrease (p<0.01) in cytotoxic reactions was observed at 3 months following the switch of patients from conventional bovine insulin preparations to ‘A’ but not to ‘B’. However in both subgroups insulin antibodies persisted for at least 12 months. Cross-reactivity between antibodies to human, porcine and bovine insulins was evident in all groups. The early cellular and humoral immune phenomena were positively correlated in both group 1A and 1B suggesting their common involvement in the pathogenesis of DM.
Key-wordsInsulin antibodies Insulin cytotoxicity Longitudinal study Type I diabetes mellitus
Unable to display preview. Download preview PDF.
- 1.Baskin B. L., Rosenthal A. S.: Determinant specific suppression of antigen induced T-cell proliferation in the guinea-pig. Quantitation of suppressed antigen-specific T-cell responses as a consequence of prior exposure to antigen in complete Freund’s adjuvant—J. Immunol.124, 184–193, 1980.PubMedGoogle Scholar
- 2.Bloom S. R., Barnes A. J., Adrian T. E., Polak J. M.: Autoimmunity in diabetics induced by hormonal contaminants of insulin—Lanceti, 14–17, 1979.Google Scholar
- 5.Fairchild R. S., Kyner J. L., Abdou N. I.: Specific immunoregulation abnormality in insulin-dependent diabetes mellitus—J. Lab. clin. Med.99, 1975–78 1982.Google Scholar
- 6.Gepts W.: Pathology of IDDM in man. In:Mngola E. N. (Ed.): Diabetes, 1982. Excerpta Medica, Amsterdam—Oxford—Princeton, 1983; pp 99–107.Google Scholar
- 18.Reeves W. G., Kelly U.: Insulin antibodies induced by bovine insulin therapy—Clin. exp. Immunol.50, 163–170, 1985.Google Scholar
- 19.Richens E. R., Luqman W., Groves R. W.: Reduced insulin binding by lymphoblastoid cell lines homozygous for HLA-DR3 and-DR4 genotypes. In:Jaworski M. A., Molnar G. D., Rajotte R. V., Singh B. (Eds): Immunology of diabetes. International Congress Series No. 717. Elsevier Science Publishers, Amsterdam, 1987; pp 263–267.Google Scholar
- 21.Richens E. R., Seward M. E., Luqman W. A., Hartog M.: The human cellular immune response to insulin: a study in unexposed control subjects and type I diabetic patients on acute and chronic treatment—J. clin. Lab. Immunol.11, 135–141, 1983.Google Scholar
- 23.Schernthaner G., Borkenstein M., Fink M., Mayr W. R., Menzel J., Schober E.: Immunogenicity of human insulin (Novo) or pork monocomponent insulin in HLA-DR typed insulin-dependent diabetic individuals. In:Karam J. H., Etzwiler D. D. (Eds): International Symposium on Human Insulin. Diabetes Care6 (Suppl. 1), 43–8, 1983.Google Scholar
- 25.Wilkin T., Armitage M., Casey C., Pyke D. A., Hoskins P. J., Rodier M., Diaz J. L., Leslie R. D. G.: Value of insulin autoantibodies as serum markers for insulin-dependent diabetes mellitus—Lanceti, 430–483, 1985.Google Scholar