1. Lymphocytes Stimulate Dehydroepiandrosterone Production through Direct Cellular Contact with Adrenal Zona Reticularis Cells: A Novel Mechanism of Immune-Endocrine Interaction1
- Author
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Stefan R. Bornstein, Tobias Lohmann, Gernot W. Wolkersdörfer, Hans-Detlef Stahl, Christian Marx, George P. Chrousos, Sabine Schröder, Robert Pfeiffer, and Werner A. Scherbaum
- Subjects
medicine.medical_specialty ,Adrenal cortex ,medicine.drug_class ,Endocrinology, Diabetes and Metabolism ,Biochemistry (medical) ,Clinical Biochemistry ,Dehydroepiandrosterone ,T lymphocyte ,Biology ,Androgen ,Biochemistry ,Androgen secretion ,Endocrinology ,medicine.anatomical_structure ,Cyclosporin a ,Internal medicine ,medicine ,Endocrine system ,Zona reticularis - Abstract
Adrenal androgen production was reduced by 80% in patients receiving T lymphocyte-suppressive medications compared to that in age-matched controls. In vitro, however, neither tacrolimus nor cyclosporin A reduced dehydroepiandrosterone (DHEA) release by adrenocortical cells. Therefore, we examined the potential role of lymphocytes in adrenal androgen production, using cocultures of human T lymphocytes and adrenocortical primary or transformed cells. Cocultures led to a 4-fold elevation of DHEA levels (490.4 ± 94.8% over basal), which was greater than the increase observed after the addition of maximal concentrations of ACTH (117.4 ± 14.8%). Separation of cells by semipermeable membranes abolished this effect, and transfer of leukocyte-conditioned medium had little androgen-stimulating effect. These data suggested that the observed stimulation of androgen secretion required cell contact rather than soluble paracrine factor(s). Furthermore, we examined human adrenal glands for the presence of T lymphocytes a...
- Published
- 1999
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