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Inhibition of Thyrotropin-Stimulated Iodide Uptake in FRTL-5 Thyroid Cells by Crude Immunoglobulin Fractions from Patients With Goitrous and Atrophic Autoimmune Thyroiditis^*

YASUTAKA TOKUDA, KANJI KASAGI, YASUHIRO IIDA, HIROTO HATABU, TAKASHI MISAKI, KEISUKE ARAI, KEIGO ENDO and JUNJI KONISHI

Department of Nuclear Medicine, Kyoto University School of Medicine Sakyo-ku, Kyoto 606, Japan

We studied the effects of crude immunoglobulin (Ig) fractions of serum from patients with goitrous and atrophic autoimmune thyroiditis on TSH-, thyroid-stimulating immunoglobulin (TSI)-, forskolin-, and dibutyryl cAMP-stimulated ¹²⁵I uptake by FRTL-5 thyroid cells. TSH-stimulated ¹²⁵I uptake was inhibited by the Ig fractions from 15 patients with atrophic thyroiditis who had serum TSH binding inhibitor Igs (TBII), 10 (62.5%) of 16 TBII-negative patients with atrophic thyroiditis, 7 (43.8%) of 16 hypothyroid patients with goitrous thyroiditis who had no TBII activity, and only 2 (15.4%) of 13 euthyroid patients with goitrous thyroiditis who were negative for TBII. The mean inhibition of TSH-stimulated ¹²⁵I uptake produced by the crude Igs from the former 3 groups of hypothyroid patients was statistically significant (P < 0.001, P < 0.001, and P < 0.01, respectively) and correlated closely with the ability of the Ig fractions to inhibit TSI-stimulated ¹²⁵I uptake (r = 0.882) and TSH-stimulated cAMP accumulation (r = 0.929). The inhibition of TSH- or TSI-stimulated ¹²⁵I uptake by Ig samples containing TBII correlated significantly with the TBII activities. On the other hand, in the presence of Igs from TBII-negative hypothyroid patients, the inhibition of TSH-stimulated l25I uptake correlated significantly with that of forskolin-stimulated ¹²⁵I uptake (r = 0.685). Although 6 (12.8%) of 47 Ig samples from hypothyroid patients inhibited dibutyryl cAMP-stimulated ¹²⁵I uptake, the activities were marginal. These findings suggest that at least 2 types of antibodies are involved in the inhibition of TSH- or TSI-stimulated ¹²⁵I uptake: 1 being a competitive inhibitor of TSH binding to its receptors, and another exerting influence on a step subsequent to TSH or TSI binding, presumably through adenylate cyclase inhibition.

^* This work was supported in part by a Research Grant for Intractable Diseases from the Ministry of Health and Welfare, Japan.

To whom requests for reprints should be addressed.

Received October 13, 1987.

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