Resolution of inflammation is an active process that is mediated in part by antiinflammatory lipid mediators. Although phospholipase A₂ (PLA₂) enzymes have been implicated in the promotion of inflammation through mobilizing lipid mediators, the molecular entity of PLA₂ subtypes acting upstream of antiinflammatory lipid mediators remains unknown. Herein, we show that secreted PLA₂ group IID (PLA2G2D) is preferentially expressed in CD11c⁺ dendritic cells (DCs) and macrophages and displays a pro-resolving function. In hapten-induced contact dermatitis, resolution, not propagation, of inflammation was compromised in skin and LNs of PLA2G2D-deficient mice (Pla2g2d^−/−), in which the immune balance was shifted toward a proinflammatory state over an antiinflammatory state. Bone marrow-derived DCs from Pla2g2d^−/− mice were hyperactivated and elicited skin inflammation after intravenous transfer into mice. Lipidomics analysis revealed that PLA2G2D in the LNs contributed to mobilization of a pool of polyunsaturated fatty acids that could serve as precursors for antiinflammatory/pro-resolving lipid mediators such as resolvin D1 and 15-deoxy-Δ^12,14-prostaglandin J₂, which reduced Th1 cytokine production and surface MHC class II expression in LN cells or DCs. Altogether, our results highlight PLA2G2D as a “resolving sPLA₂” that ameliorates inflammation through mobilizing pro-resolving lipid mediators and points to a potential use of this enzyme for treatment of inflammatory disorders.