Immunology in diabetes: an update.

Immunology in diabetes: an update.

Immunology in diabetes: an update.

Abstract

Summary. Type 1 (insulin-dependent) diabetes mellitus is strongly associated with autoimmune
phenomena connected to the loss of b-cells in the pancreatic islets. Despite considerable progress
in our understanding of genetic susceptibility factors and islet autoimmunity preceding the
clinical onset of Type 1 diabetes there are considerable gaps in our knowledge. First, the etiology
is unclear. It is speculated that multiple etiological factors may initiate a common pathogenic
pathway which results in immune-mediated b-cell destruction. In 1998 we will need to learn
more about the possible importance of gestational infections, as well as isolation of viral DNA
or RNA from the blood of new-onset patients or marker-positive individuals. The scan of the
whole genome has provided a smorgasbord of genetic regions which confer diabetes risk either
alone or in combination. HLA remains the major genetic risk factor, and while HLA peptide
binding information is considerable, we understand less of autoantigen processing and presentation. Cloned autoantigens and their use in standardized autoantibody assays have improved
our ability to identify individuals at risk for diabetes. The diagnostic sensitivity and specificity
of autoantibody markers for Type 1 diabetes are high as are their predictive values. We need
methods to combine autoantibodies with genetic risk factors. The identification of individuals in
different stages of their pathogenesis, including patients with so-called slowly progressive Type 1
diabetes (SPIDDM, LADA etc.), allow approaches to novel therapeutic interventions. Insulin is
currently the therapeutic agent of choice and although spontaneous insulin-dependent diabetes
in the NOD mouse and the BB rat can be prevented by immune suppression or modulation,
this has not yet been possible in humans. The 1998 research on the interaction between
environmental factors and susceptibility genes to initiate b-cell specific autoreactivity should
allow the development of therapies for prevention, and perhaps a cure, of insulin-dependent
(Type 1) diabetes.

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