Modulation by thymus-derived (T) cells of thyroid cell-stimulated prostaglandin E release by human peripheral blood mononuclear cells.

Abstract
Cultures of plastic-adherent, human peripheral blood mononuclear cells generated prostaglandin (PGE). Culture of adherent cells (predominantly monocytes) with human thyroid cells enhanced PGE accumulation in the medium, although to a lesser degree than occurs with unseparated blood mononuclear cells. Recombination of the adherent cells with monocyte-depleted, nonadherent cells restored basal and thyroid cell-stimulated PGE generation to the levels seen with unseparated cells. Thymus derived (T) cells obtained by rosetting with sheep erythrocytes enhanced the adherent cell basal PGE production and the increased PGE accumulation that occurs in the presence of thyroid cells (50-120% augmentation by the T cells). Significant augmentation of thyroid cell-stimulated PGE release by 105 adherent cells occurred with the addition of as few as 5 .times. 104 T cells. Culture medium transfer experiments and separation of cell types during culture by a semipermeable membrane provided evidence against the possibility that adherent cells were releasing a factor that stimulated T cell PGE generation or that T cells were releasing a factor that enhanced adherent cell PGE generation. This T cell effect apparently requires direct contact with adherent cells. Human T cells are important in the release by adherent cells of PGE, a mediator of suppressor function by some immune cells.

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