ArticleClinical and experimental immunology1995
Brain-reactive autoantibodies in BB/d rats do not recognize glutamic acid decarboxylase.
Article in Clinical and experimental immunology, 1995. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 8 citations in OpenAlex.
- Distinct antigenic features of linear epitopes at the N-terminus and C-terminus of 65 kDa glutamic acid decarboxylase (GAD65): implications for autoantigen modification during pathogenesis.Clinical and experimental immunology · 2002Article
- Islet glutamic acid decarboxylase modified by reactive oxygen species is recognized by antibodies from patients with type 1 diabetes mellitus.Clinical and experimental immunology · 2001Article
- Heterogeneity in the occurrence of a subset of autoantibodies to glutamic acid decarboxylase in autoimmune polyendocrine patients with islet cell antibodies.Clinical and experimental immunology · 1998Article
- GABAergic neurons in barrel cortex show strong, whisker-dependent metabolic activation during normal behavior.The Journal of neuroscience : the official journal of the Society for Neuroscience · 1997Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The BB rat spontaneously develops insulin-dependent diabetes mellitus (IDDM) similar to that in humans. The most practical markers of beta cell autoimmunity are circulating antibodies to islet cell components. In particular autoantibodies to the enzyme glutamic acid decarboxylase (GAD) are a common feature of IDDM development in humans. This study aims at investigating the prevalence and levels of autoantibodies in BB rats to antigens in a semipurified, GAD-enriched preparation from rat brain. Eighteen diabetes-prone BB/d rats (10 male and eight female) were tail bled weekly from age 28 days to 113 days and antibodies detected on the rat brain preparation by ELISA. Antibody levels were expressed as arbitrary units relative to a standard positive serum. Individual rats varied in the time and order of antibody appearance and IDDM onset, with the earliest occurrence being 42 days and 69 days, respectively. In some rats antibody production was maintained but declined in others. By 113 days 85% of diabetic rats had at some time been positive for autoantibodies to brain components, compared with 25% of non-diabetics (P = 0.09 by Fisher's exact test). Immunoabsorption studies using recombinant rat GAD-65 or recombinant human GAD-67 failed to inhibit the binding of BB rat sera to the original rat brain preparation. A capture ELISA using GAD-6 MoAb to capture GAD-65 from rat brain preparation or from a preparation of recombinant rat GAD-65, failed to detect anti-GAD antibodies in BB rats. Immunofluorescent staining of tissue sections showed the autoantibodies to be brain-specific, but having distinct staining patterns to the anti-GAD antibodies of Stiff Man Syndrome serum. In conclusion, BB rats possess autoantibodies reactive with rat brain antigens which may be associated with IDDM. However, these are not directed against GAD.
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