IMMUNOGLOBULIN-G THAT INTERFERES WITH THYROID-STIMULATING ANTIBODY MEASUREMENTS CAN BE ELIMINATED SPECIFICALLY BY INCUBATION WITH SYNTHETICPEPTIDES CORRESPONDING TO PARTIAL SEQUENCES OF THE HUMAN THYROTROPIN RECEPTOR
Y. Ueda et al., IMMUNOGLOBULIN-G THAT INTERFERES WITH THYROID-STIMULATING ANTIBODY MEASUREMENTS CAN BE ELIMINATED SPECIFICALLY BY INCUBATION WITH SYNTHETICPEPTIDES CORRESPONDING TO PARTIAL SEQUENCES OF THE HUMAN THYROTROPIN RECEPTOR, Thyroid, 3(2), 1993, pp. 111-117
Two IgG preparations out of more than 100 tested, distinct from the ty
pical Graves' disease IgG, were shown specifically to enhance the cAMP
production of FRTL-5 cells by the addition of a synthetic peptide, P-
218, corresponding to the partial amino acid sequence from No. 354 to
367 of the h thyroid-stimulating hormone (TSH) receptor. IgG obtained
from a patient with Graves' disease revealed a serial alteration of th
e enhancement; negative in July, 1989, potent in January, 1991, and we
ak in September 1991. During this time there was no remarkable change
in the patient's serum protein components or TSH receptor antibody act
ivities. A peptide with a completely reverse sequence of P-218 showed
little effect, and P-218 in combination with bTSH or forskolin did not
affect cAMP production by these ligands, and did not alter the inhibi
tory activity of thyroid-stimulation-blocking antibody. High concentra
tions of P-218 resulted in reduction of such enhancing effects of cAMP
by thyroid-stimulating antibody. P-218 affinity chromatography showed
almost complete absorption and recovery of thyroid-stimulating antibo
dy and P-218 reactivity. In the 15 synthesized peptides with proximal
sequences of P-218 (from 338 to 378), regions thought to be involved w
ith the enhancement were defined as follows: 354-367 (P-218) is a crit
ical unit; 354-357 and 364-367 are considered to be the essential site
s; several amino acid extensions on both N- and C-terminal sides of P-
218 show additional enhancement. In conclusion, evidence was shown to
indicate the presence of IgG that interferes with thyroid-stimulating
antibody measurements.