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These seemingly contradictory findings are not uncommon given that COX-2 induction by tissue injuries leads to syntheses of five different prostanoids that act on a total of nine GPCRs to mediate both pro- and anti-inflammatory effects [140], although COX-2-derived PGE 2 is primarily responsible for its pathogenic roles in both the CNS and periphery [135, 156]

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Different subsets of DCs are involved in activating T-cell immunity, causing anergy and mediating inflammation is a subject of wide research interest (143, 144, 146)