Conversion of TBAb Response to TSAb Response by Anti-human IgG Antibody

Title:Conversion of TBAb Response to TSAb Response by Anti-human IgG Antibody

Volume: 13 Issue: 4

Author(s): Yukio Ochi, Yoshihiro Kajita, Takashi Hachiya, Naoko Arata and Masaru Hamaoki

Affiliation:

Keywords: Cyclic AMP, Graves’ disease, Primary hypothyroidism, TBAb, TBII, TSAb.

Abstract: Previously, we reported the conversion phenomenon (CP) of thyroid blocking antibody (TBAb) to thyroid stimulating antibody (TSAb) by induced cAMP production during incubation of TBAb-bound porcine thyroid cells (PTC) with rabbit anti-IgG Ab. In the present experiment we examined the CP by TBAb-positive sera with high TSH binding inhibitor immunoglobulin (TBII) activity in primary hypothyroidism. Two patients with extremely high TBII patients; patient No.1 (35 yo male) with TSH 26.5μU/ml, TSAb negative, TBII 4,600 U/L, TBAb100% and patient No.2 (40 yo female) with TSH 4.5μU/ml, TSAb negative, TBII 1,620 U/L, TBAb 99.8% were examined. Cyclic AMP production was examined by 2nd incubation (3h) of anti-IgG Ab with TBAb-bound PTC that was made by 1st incubation (0.5h) of TBAbpositive serum and PTC. When sera (0.001-0.05 ml) of patient No.1 and No.2 were tested, cAMP production showed 980- 3,700% and 570-3,000% in a dose-dependent manner, respectively. Cyclic AMP production was also observed by anti- IgG fragments Ab [(Fab’)₂, Fab and light chain]. Cyclic AMP production by anti-F(ab’)₂ was higher than anti-Fab Ab, and cAMP by anti-κ Ab was significantly higher (>3 fold) than anti-λ Ab. Cyclic AMP production by TBAb-positive sera with high TBII activity (35-270 U/L) showed a correlation with serum TBII activity (R=0.76). The fact that all high TBAb-positive sera show the CP of TBAb to TSAb suggests that TSAb activity may be present in TBAb molecule and TBAb may be the precursor of TSAb.

Cite this article as:

Ochi Yukio, Kajita Yoshihiro, Hachiya Takashi, Arata Naoko and Hamaoki Masaru, Conversion of TBAb Response to TSAb Response by Anti-human IgG Antibody, Endocrine, Metabolic & Immune Disorders - Drug Targets 2013; 13 (4) . https://dx.doi.org/10.2174/1871530313666131224115000