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Heat-shock protein 65 as a beta cell antigen of insulin-dependent diabetes

D B Jones1, N R Hunter, G W Duff

  • 1Department of Medicine, Western General Hospital, Edinburgh, UK.

Lancet (London, England)
|September 8, 1990
PubMed

Insights

Heat-shock protein 65 (HSP65) from Mycobacterium tuberculosis may be the primary beta-cell antigen in insulin-dependent diabetes. Autoimmunity to HSP65 might increase susceptibility to this autoimmune disease.

Area of Science:

  • Immunology
  • Endocrinology
  • Microbiology

Background:

  • The primary beta-cell antigen in insulin-dependent diabetes is a ~64 kD protein.
  • Insulinoma cells synthesize this 64 kD protein upon stimulation with hyperthermia and cytokines like interleukin-1 beta, gamma interferon, and tumor necrosis factor.

Purpose of the Study:

  • To investigate the identity of the 64 kD beta-cell antigen.
  • To explore the potential role of heat-shock proteins in the pathogenesis of insulin-dependent diabetes.

Main Methods:

  • Western blot analysis was used to assess cross-reactivity between the 64 kD beta-cell protein and antibodies against heat-shock protein 65 (HSP65) from Mycobacterium tuberculosis and Mycobacterium leprae.
  • Inhibition assays were performed using serum from insulin-dependent diabetic patients.

Main Results:

  • Cross-reactivity was observed between the 64 kD beta-cell protein and antibodies against Mycobacterium tuberculosis HSP65, but not against Mycobacterium leprae HSP65.
  • Serum from insulin-dependent diabetic patients, containing antibodies to the 64 kD beta-cell antigen, inhibited the binding of Mycobacterium tuberculosis HSP65 antibodies to cytokine-treated cells.

Conclusions:

  • Heat-shock protein 65 (HSP65) is suggested to be the 64 kD beta-cell antigen.
  • Autoreactivity to an epitope of HSP65 may confer susceptibility to insulin-dependent diabetes mellitus.

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