MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-II EXPRESSION AND PARATHYROID AUTOANTIBODIES IN PRIMARY HYPERPARATHYROIDISM

Citation
G. Bjerneroth et al., MAJOR HISTOCOMPATIBILITY COMPLEX CLASS-II EXPRESSION AND PARATHYROID AUTOANTIBODIES IN PRIMARY HYPERPARATHYROIDISM, Surgery, 124(3), 1998, pp. 503-509
Citations number
36
Categorie Soggetti
Surgery
Journal title
ISSN journal
00396060
Volume
124
Issue
3
Year of publication
1998
Pages
503 - 509
Database
ISI
SICI code
0039-6060(1998)124:3<503:MHCCEA>2.0.ZU;2-P
Abstract
Background. Autoimmune diseases are characterized by induced parenchym al expression of major histocompatibility complex (MHC) class II antig ens and circulating autoantibodies directed toward surface structures on the target cells. MHC class II expression can be modified by viral infections of potential pathogenic importance in autoimmune reactions. Primary hyperparathyroidism exhibits an incompletely clarified cause. Methods. With cryosections, human parathyroid glands were stained wit h monoclonal antibodies to MHC class II antigens according to a peroxi dase-antiperoxidase technique. Human parathyroid adenoma tissue transp lanted to nude mice and rat parathyroid glands was tested with serum f rom patients with hyperparathyroidism and control subjects. Results. I nduced MHC class II expression was demonstrated on parathyroid parench ymal cells in 13 of 54 adenomatous and eight of 23 hyperplastic glands of patients with primary hyperparathyroidism. This reactivity was abs ent in 12 normal glands, nine normal-sized glands associated with the adenomas, and 17 enlarged glands of patients with hyperparathyroidism caused by uremia. Staining of parathyroid tissue was found with serum from 27 of 38 patients with primary hyperparathyroidism, whereas this reactivity was absent on rat thyroid and pancreatic tissue, as well as with control sera. Conclusions. The concurrent induction of MHC class II antigen expression and circulating antiparathyroid autoantibodies in 16 of 38 patients with primary hyperparathyroidism suggests hithert o unrecognized immunologic involvement in this disease.