Functions as a positive regulator of osteoclastogenesis (PubMed:19251634). Cell surface receptor that signals via TYROBP (PubMed:10449773). Regulates inflammatory responses (PubMed:20212065). Monomer (By similarity). Homodimer (By similarity). The majority of CLEC5A is expressed as a monomeric form on macrophages (By similarity). Interacts with TYROBP/DAP12 (PubMed:10449773). The interaction with TYROBP is required for CLEC5 cell surface expression (PubMed:10449773). Interacts with HCST/DAP10 (PubMed:19074552, PubMed:19251634). Forms a CLEC5A/TYROBP/HCST trimolecular complex depending almost solely on TYROBP (PubMed:19251634). Strong expression in bone marrow cells and thioglycollate-induced neutrophils (at protein level) (PubMed:19074552). Expressed on granulocytes and monocytes from bone marrow and peripheral blood (PubMed:20212065). Expressed in macrophage cell line J-774, but not in T-cell lines, B-cell lines, or mast cell lines (PubMed:10449773). By TNF in bone-marrow derived macrophage colony-stimulating factor-dependent macrophages (PubMed:20212065). Up-regulated during the differentiation of myeloid cell line 32Dcl3 into neutrophils (PubMed:19074552). N-glycosylated (PubMed:19074552, PubMed:19251634). Contains sialic acid residues (PubMed:19074552). Involved in the pathogenetic mechanisms of Japanese encephalitis virus (JEV) infection of the brain. JEV infection of young mice results in increased expression of CLEC5A in spleen and brain with consequent activation of proinflammatory cytokine secretion. Mutants are viable, are born in the expected Mendelian ratios and have similar numbers of myeloid and lymphoid cell subsets as wild-type animals (PubMed:20212065). Inhibition of autoimmune joint inflammation and preservation of bone density (PubMed:20212065). Acts as a key regulator of synovial injury and bone erosion during autoimmune joint inflammation when its activation leads to enhanced recruitment of inflammatory macrophages and neutrophils to the joints. MDL-1