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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: BACKGROUND, METHODS, RESULTS. Meshes: Animals, Cell Proliferation, Cells, Cultured, Down-Regulation, Hypersensitivity, Delayed, Immunization, Interleukin-17, Lymphocyte Activation, Male, Mice, Mice, Inbred BALB C, Mice, Knockout, Th17 Cells, Th2 Cells.
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Is development of IL-17-mediated delayed-type hypersensitivity affected by down-regulation of IL-25 expression? Context: IL-25, which is a member of the IL-17 family, induces Th2 cell differentiation and Th2 cytokine production, contributing to induction of Th2-type immune responses and diseases, as a result of which it suppresses Th1- and Th17-type immune responses. To elucidate the role of IL-25 in the pathogenesis of IL-17-mediated delayed-type hypersensitivity (DTH), IL-25-deficient mice were sensitized with methylated BSA (mBSA), and then a DTH reaction was induced by mBSA challenge. mBSA-specific T-cell induction was assessed on the basis of cell proliferation and cytokine production. The DTH reaction was evaluated on the basis of tissue swelling, histology and inflammatory mediator expression. IL-25 expression was markedly reduced in local DTH lesions. However, mBSA-specific Th1, Th2 and Th17 cell induction, and the mBSA-induced DTH reaction were comparable in IL-25-deficient and wild-type mice.
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IL-25 is not essential for differentiation of Th1, Th2 and Th17 cells in the sensitization phase or induction of local inflammation in the elicitation phase of the mBSA-induced DTH reaction. Final Decision: no