Effect of thyroid hormones and other iodinated compounds on the transition of monocytes into veiled/dendritic cells: role of granulocyte-macrophage colony-stimulating factor, tumour-necrosis factor-α and interleukin-6

Author:

Mooij P,Simons P J,de Haan-Meulman M,de Wit H J,Drexhage H A

Abstract

Abstract Stimulation of human peripheral blood monocytes with the thyroid hormones tri-iodothyronine (T3) and thyroxine (T4) enhanced their ability to mature into cytologically and functionally characteristic veiled/dendritic cells. Veiled/dendritic cell transition induced by T3 and T4 was dependent on the production of granulocyte-macrophage colony-stimulating factor (GM-CSF), tumour necrosis factor-α (TNFα) and interleukin-6 (IL-6) in the culture, since the addition of antibodies specific for GM-CSF, TNFα and IL-6 to the culture system had blocking effects. The addition of antibodies to macrophage colony-stimulating factor and IL-1 had no effects. Contaminating T cells and B cells did not contribute to the transition of monocytes to veiled/dendritic cells, and it is therefore likely that the GM-CSF, TNFα and IL-6 produced in the culture system were derived from the monocytes themselves. Stimulation of the blood monocytes with an optimal concentration of metrizamide (14·5%), reverse T3 (rT3; 2 × 10−10 m) or highly iodinated thyroglobulin (Tg; 2 × 10−11 m) also resulted in an increased transition of monocytes to veiled/dendritic cells, but to a lesser extent in comparison with the thyroid hormones (T3, 31 ±6% and T4, 25 ±5% vs rT3, 22 ± 8% and Tg with an iodination grade of 0·37%: 20 ± 4% veiled/dendritic cells). Administration of anti-GM-CSF, anti-TNFα and anti-IL-6 to the culture system also had blocking effects on the transition from monocytes to veiled/dendritic cells induced by the iodinated compounds. The mechanisms by which such iodinated compounds act on the monocyte to veiled/dendritic cell transition can only be speculated on (interference H2O2-generating system?). Journal of Endocrinology (1994) 140, 503–512

Publisher

Bioscientifica

Subject

Endocrinology,Endocrinology, Diabetes and Metabolism

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