Secretory calcium-dependent phospholipase A2 that primarily targets extracellular lipids, exerting anti-inflammatory and immunosuppressive functions (PubMed:10531313, PubMed:23690440, PubMed:26392224, PubMed:10455175). Hydrolyzes the ester bond of the fatty acyl group attached at sn-2 position of phospholipids (phospholipase A2 activity) with preference for phosphatidylethanolamines and phosphatidylglycerols over phosphatidylcholines (By similarity). In draining lymph nodes, selectively hydrolyzes diacyl and alkenyl forms of phosphatidylethanolamines, releasing omega-3 polyunsaturated fatty acids (PUFAs) such as eicosapentaenoate and docosahexaenoate that are precursors of the anti-inflammatory lipid mediators, resolvins (PubMed:23690440). During the resolution phase of acute inflammation drives docosahexaenoate-derived resolvin D1 synthesis, which suppresses dendritic cell activation and T-helper 1 immune response (PubMed:23690440, PubMed:27226632). May act in an autocrine and paracrine manner. Via a mechanism independent of its catalytic activity, promotes differentiation of regulatory T cells (Tregs) and participates in the maintenance of immune tolerance (PubMed:19564598). May contribute to lipid remodeling of cellular membranes and generation of lipid mediators involved in pathogen clearance. Displays bactericidal activity against Gram-positive bacteria by directly hydrolyzing phospholipids of the bacterial membrane (PubMed:11694541). a 1,2-diacyl-sn-glycero-3-phosphoethanolamine + H2O = a 1-acyl-sn-glycero-3-phosphoethanolamine + a fatty acid + H(+) 1-hexadecanoyl-2-(9Z-octadecenoyl)-sn-glycero-3-phosphoethanolamine + H2O = (9Z)-octadecenoate + 1-hexadecanoyl-sn-glycero-3-phosphoethanolamine + H(+) 1-hexadecanoyl-2-(9Z,12Z-octadecadienoyl)-sn-glycero-3-phosphoethanolamine + H2O = (9Z,12Z)-octadecadienoate + 1-hexadecanoyl-sn-glycero-3-phosphoethanolamine + H(+) 1,2-dihexadecanoyl-sn-glycero-3-phospho-(1'-sn-glycerol) + H2O = 1-hexadecanoyl-sn-glycero-3-phospho-(1'-sn-glycerol) + H(+) + hexadecanoate 1-hexadecanoyl-2-(9Z-octadecenoyl)-sn-glycero-3-phospho-(1'-sn-glycerol) + H2O = (9Z)-octadecenoate + 1-hexadecanoyl-sn-glycero-3-phospho-(1'-sn-glycerol) + H(+) a 1,2-diacyl-sn-glycero-3-phosphocholine + H2O = a 1-acyl-sn-glycero-3-phosphocholine + a fatty acid + H(+) 1,2-dihexadecanoyl-sn-glycero-3-phosphocholine + H2O = 1-hexadecanoyl-sn-glycero-3-phosphocholine + H(+) + hexadecanoate 1-hexadecanoyl-2-(9Z-octadecenoyl)-sn-glycero-3-phosphocholine + H2O = (9Z)-octadecenoate + 1-hexadecanoyl-sn-glycero-3-phosphocholine + H(+) 1-hexadecanoyl-2-(9Z,12Z-octadecadienoyl)-sn-glycero-3-phosphocholine + H2O = (9Z,12Z)-octadecadienoate + 1-hexadecanoyl-sn-glycero-3-phosphocholine + H(+) 1-hexadecanoyl-2-(4Z,7Z,10Z,13Z,16Z,19Z-docosahexaenoyl)-sn-glycero-3-phosphocholine + H2O = (4Z,7Z,10Z,13Z,16Z,19Z)-docosahexaenoate + 1-hexadecanoyl-sn-glycero-3-phosphocholine + H(+) Binds 1 Ca(2+) ion per subunit. Localizes to cell membrane likely through binding to heparan sulfate proteoglycans. Highly expressed in secondary lymphoid tissues, spleen and lymph nodes. Expressed at a lesser extent in thymus (PubMed:11196711, PubMed:10455175, PubMed:10531313, PubMed:23690440). Expressed in CD4-positive, IL2RA/CD25-positive, FOXP3-positive Tregs (at protein level) (PubMed:19564598, PubMed:23690440). Expressed in myeloid cell subsets resident in spleen and lymph nodes, ITGAX/CD11C-positive dendritic cells and macrophages (at protein level). Enriched in CD4-positive, ITGAM/CD11B-positive dendritic cell subset (PubMed:19564598, PubMed:23690440). Expressed in pulmonary ITGAX/CD11C-positive dendritic cell subset (at protein level) (PubMed:26392224). Undetectable in embryonic spleens. Weak expression is detected the first week after birth, with further increase to normal levels by 4-6 weeks after birth. Up-regulated in thymus upon endotoxin challenge (PubMed:10455175). Up-regulated during Treg differention in response to TGFB1 (PubMed:19564598). Up-regulated in pulmonary ITGAX/CD11C-positive dendritic cell subset upon chronic oxidative stress associated with aging (PubMed:26392224). Knockout mice are born at the expected Mendelian rate and have normal embryonic and postnatal development (PubMed:23690440). They are susceptible to acute and chronic inflammatory reactions and resistant to tumorigenesis. In a model of hapten-induced contact hypersensitivity, mutant mice show an enhanced T-helper 1 immune response in skin lymph nodes at sensitization phase followed by delayed inflammation resolution with more severe ear swelling, epidermal hyperplasia, and inflammatory cell infiltration at elicitation phase (PubMed:23690440, PubMed:27226632). In a psoriasis model, mutant mice show enhanced T-helper 17 immune response and epidermal hyperplasia associated with decreased synthesis of omega-3 PUFAs (PubMed:27226632). In a model of chemically-induced skin carcinogenesis, mutant mice show resistance to cutaneous papilloma formation (PubMed:27226632). In response to SARS-CoV infection, mutant middle-aged (10-13 month old) mice mount a potent antiviral T cell response, resulting in more rapid virus clearance and significantly decreased mortality compared with wild-type ones. This represents a relevant model for SARS-CoV increased susceptibility with aging in human (PubMed:26392224). Belongs to the phospholipase A2 family.