TCD4 cells play a critical role in the immune adaptive response as well as in activation of innate immune cells. The cytokines signature produced by these cells, the transcriptions factors and their effector functions, these lymphocytes are subdivided in different populations: Th1, Th2, Th9, Th17 e Treg. These T cells subsets play a key role in the elimination of fungi and bacteria by (Th1/Th17), viruses (Th1) and helminths (Th2/Th9), as well as tissue injury observed in the autoimmune disease (Th1/Th17).However, this classification of well defined subtypes of lymphocytes T helper: Th1, Th2, Th9, Th17 e Treg has been discussed in the latest years. Several groups have demonstrated that Th cells co-expressing IL-17 and IFN-g might indicate a potential plasticity of Th1 and Th17 cells. Recently, our group have found that the phagocytosis of infected apoptotic cell by dendritic cells promote the synthesis of different cytokines such as: TGF-², IL-6, IL-1² e IL-1±, as well as the production of PGE2. These soluble mediators derived from phagocytosis of infected apoptotic cells promote the differentiation of Th17 cells, however a small percentage of IFN-g-producing cells have also been observed. It is known that besides those cytokines, lipid mediators as PGE2 plays a key role in the differentiation of Th1, Treg and Th17 cells. Similarly, the plasticity of these subpopulations seems to be directly related to the balance of cytokines in the microenvironment. However, until now, nothing has been described about the role of PGE2 in the plasticity of Th17 to different subpopulations of T cells.
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