Major histocompatibility complex class II expression and parathyroid autoantibodies in primary hyperparathyroidism
Background: Autoimmune diseases are characterized by induced parenchymal expression of major histocompatibility complex (MHC) class II antigens and circulating autoantibodies directed toward surface structures on the target cells. MHC class II expression can be modified by viral infections of potent...
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Veröffentlicht in: | Surgery 1998-09, Vol.124 (3), p.503-509 |
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Sprache: | eng |
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Zusammenfassung: | Background: Autoimmune diseases are characterized by induced parenchymal expression of major histocompatibility complex (MHC) class II antigens 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 with monoclonal antibodies to MHC class II antigens according to a peroxidase-antiperoxidase technique. Human parathyroid adenoma tissue transplanted to nude mice and rat parathyroid glands was tested with serum from patients with hyperparathyroidism and control subjects.
Results: Induced MHC class II expression was demonstrated on parathyroid parenchymal cells in 13 of 54 adenomatous and eight of 23 hyperplastic glands of patients with primary hyperparathyroidism. This reactivity was absent 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 hitherto unrecognized immunologic involvement in this disease. (Surgery 1998;124:503-9.) |
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ISSN: | 0039-6060 1532-7361 |
DOI: | 10.1016/S0039-6060(98)70096-0 |