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- Title
An RT6a gene is transcribed and translated in lymphopenic diabetes-prone BB rats.
- Authors
Crisá, Laura; Sarkar, Probir; Waite, Debra J.; Friedrich, Friedrich Haag; Koch-Nolte; Rajan, T. V.; Mordes, John P.; Handler, Eugene S.; Thiele, Heinz-Günter; Rossini, Aldo A.; Greiner, Dale L.; Crisá, L; Sarkar, P; Waite, D J; Friedrich, F H; Mordes, J P; Handler, E S; Thiele, H G; Rossini, A A
- Abstract
T-cells expressing the RT6 surface alloantigen appear to perform important immunoregulatory functions in the rat. Diabetes-prone BB rats lack circulating RT6+ T-cells and spontaneously develop autoimmune diabetes mellitus and thyroiditis. The coisogenic diabetes-resistant BB rat does circulate RT6+ T-cells and is free of disease. Transfusions leading to engraftment of RT6+ T-cells prevent both diabetes and thyroiditis in the diabetes-prone rat. To investigate the absence of this subset in the lymphopenic BB rat, we used both molecular and biochemical procedures and made the following observations: 1) an mRNA encoding RT6 protein is present in diabetes-prone spleen cells; 2) nucleotide sequencing of this transcript reveals an intact coding sequence for the RT6.1 alloantigen; 3) sensitive chemiluminescent assay of diabetes-prone lymph node cell detergent extracts shows that diabetes-prone RT6 mRNA is translated in vivo; 4) quantitatively, diabetes-prone lymph node cells express < or = 10% of the RT6.1 protein found on similar numbers of diabetes-resistant BB cells; and 5) finally, we obtained evidence of an intact phosphatidylinositol linkage of the molecule to the cell surface and successfully immunoprecipitated the phosphatidylinositol-linked protein with DS4.23 monoclonal antibody, indicating that the RT6.1 antigen is correctly processed and folded in diabetes-prone lymph node cells. We conclude that the near total absence of RT6+ T-cells in the diabetes-prone BB rat is unlikely to be because of a defect in RT6 gene expression per se. Defects in RT6 gene regulation or other cellular defects leading to premature cell death in the T-cell lineage, alone or in combination, may instead be responsible.
- Publication
Diabetes, 1993, Vol 42, Issue 5, p688
- ISSN
0012-1797
- Publication type
journal article
- DOI
10.2337/diab.42.5.688