Both thyrocytes and polymorphonuclear granulocytes (PMNs) are known to have on their surface
thyrotropin receptor (TSH-R). Anti-TSH-R
antibodies having stimulating and blocking effects on thyroid function have been detected in sera of Graves' patients. Thyroid stimulating anti-TSH-R
antibodies (TSAb) are involved in the pathomechanism of
thyrotoxicosis. The basic question is in this study whether TSAb exerts effects on metabolic activity of PMNs.
Immunoglobulin G (IgGs) of 32 patients with
thyrotoxicosis had significant inhibitory effect (p less than 0.001) on chemiluminescence of healthy PMNs compared to controls. An inverse correlation was observed between inhibitory effect of IgGs on function of PMNs and TT4 (r = -0.61) in contrast to anti-
TSH-receptors antibodies (r = 0.09). TSAbs of eight
hyperthyroid patients were measured by determination of
cyclic AMP in
suspension and slices of porcine thyroid gland. Function of human PMNs separated from healthy donors was determined by
luminol-amplified chemiluminescence. Photon-emission of PMNs induced by adherence was significantly lower than that of controls. None of patients' IgGs contained anti-PMNs
antibodies or other toxic compounds. It was found an inverse correlation between chemiluminescence of PMNs and capability of TSAb to increase intracellular cAMP in thyroid slices and the
thyroid hormone levels of patients with
thyrotoxicosis (p = 0.0005). In conclusion, TSH-R on PMNs did not belong to "mute" receptors and metabolic changes in PMNs induced by TSAb might have pathogenetic as well as methodological implications.