IL-12-deficient dendritic cells, generated in the presence of prostaglandin E2, promote type 2 cytokine production in maturing human naive T helper cells.

摘要: We studied to what extent the presence of an inflammatory mediator PGE2, during development dendritic cells (DC) affects their subsequent ability induce Th1- and Th2-type cytokines in maturing naive Th cells. PGE2 (10(-9)-10(-6) M) did not alter morphology or expression class II MHC costimulatory molecules on DC obtained from monocytes granulocyte-macrophage CSF IL-4, although at concentrations above 10(-8) M, prevented acquisition CD1a marker. Both control (PGE2-DC) were potent stimulators In contrast DC, which produced high amounts IL-12 trace IL-10, PGE2-DC no IL-10 when stimulated absence PGE2. This distinct cytokine profile was stable for least 48 h additional culture Control induced Th0-like superantigen-activated cells, whereas promoted that IL-4 IL-5. Experiments using IL-12-neutralizing Abs rIL-12 indicated a crucial role deficiency induction type 2 profiles. These findings suggest elevated levels promote responses by stably impairing produce IL-12. Since are protective several Th1-related autoimmune disorders, may be considered use immunotherapy.