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TSH RECEPTOR ANTIBODY INDUCTION OF THYROGLOBULIN RELEASE FROM HUMAN THYROID CELL MONOLAYERS
Author(s) -
FELDMAN A.,
SCHWARTZ A. E.,
FRIEDMAN E. W.,
DAVIES T. F.
Publication year - 1986
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1986.tb03594.x
Subject(s) - thyroglobulin , endocrinology , medicine , receptor , antibody , thyroid , thyrotropin receptor , basal (medicine) , chemistry , in vitro , monoclonal antibody , cell surface receptor , graves' disease , immunology , biochemistry , diabetes mellitus
SUMMARY We investigated the influence of TSH receptor antibody (TRA), as detected by inhibition of 125 I‐bTSH binding to detergent solubilized porcine TSH receptors, on in‐vitro thyroglobulin (hTg) production using normal thyroid cells in monolayer. Secretion of hTg into the culture medium was analysed by a noncompetitive enzyme immunosorbent (ELISA) technique utilizing two murine monoclonal antibodies. Basal hTg release (mean ± SD 124 ± 27 ng/10 5 cells/6 d, n = 5) was stimulated by bTSH (10, 10 2 , 10 3 μU/ml) in a dose related manner (mean ± SD 191 ±24, 587 ±80, 695 ±66 ng/10 5 cells/6 d, respectively). IgG (2 mg/ml) from seven patients with hyperthyroid Graves' disease, and known titres of TRA, similarly enhanced production of hTg, in a dose and time‐dependent manner, when compared to control IgG. The degree of induction varied from a 140–230% increase in total hTg release over a 6‐day incubation period. There was a direct correlation between the degree of 125 I‐bTSH binding inhibitory activity and the hTg response ( r = 0.9, P < 001). These data demonstrate that TSH receptor antibodies enhance hTg release from human thyroid cell monolayers and allow an assessment to be made of antibody‐activated post receptor mechanisms.