Probable cell surface receptor that plays several roles in cellular fusion, cell differentiation, bone and immune homeostasis. Plays a role in TNFSF11-mediated osteoclastogenesis. Cooperates with OCSTAMP in modulating cell-cell fusion in both osteoclasts and foreign body giant cells (FBGCs). Participates in osteoclast bone resorption. Involved in inducing the expression of tartrate-resistant acid phosphatase in osteoclast precursors. Plays a role in haematopoietic stem cell differentiation of bone marrow cells toward the myeloid lineage. Inhibits the development of neutrophilic granulocytes. Plays also a role in the regulation of dendritic cell (DC) antigen presentation activity by controlling phagocytic activity. Involved in the maintenance of immune self-tolerance and avoidance of autoimmune reactions. Interacts with CREB3 (By similarity). Monomer. Homodimer. Isoform 1 interacts (via the C-terminus cytoplasmic tail) with OS9 isoform 1 (via the C-terminus tail); the interaction induces DCSTAMP redistribution to the endoplasmic reticulum-Golgi intermediate compartment. Isoform 1 interacts (via the C-terminus cytoplasmic tail) with OS9 isoform 2 (via the C-terminus tail). Localized to the cell surface in osteoclasts and undifferentiated monocytes. Intracellular internalized DCSTAMP is detected in a fraction of RANKL-induced osteoclast precursor. Colocalizes with OS9 in the endoplasmic reticulum (ER) of immature dendritic cell (DC). Translocates from the endoplasmic reticulum to the intermediate/Golgi compartment upon maturation of DC in a OS9-dependent manner. Colocalizes with LAMP1 in endosomes. Expressed in macrophages and bone marrow dendritic cells (BM-DC). Weakly expressed in the spleen and lymph node. Highly expressed in multi-nuclear osteoclasts compared to mono-nuclear macrophages. Expressed in foreign body giant cells (FBGCs). Isoform 1 and isoform 2 are expressed in osteoclasts. Up-regulated by IL4/interleukin-4, macrophage colony-stimulating factor (M-CSF), receptor activator of NF-KB ligand (RANKL), lipopolysaccharide (LPS) and toll-like receptor (TLR). Up-regulated by TNFSF11-induced osteoclast differentiation in combination with TNF-alpha. Down-regulated upon dendritic cell (DC) maturation. Several domains are necessary for interacting with OS9. The region in the cytoplasmic tail that is necessary for interaction with OS9, is also required for its transport. Glycosylated. Mice show a lack of osteoclast and foreign body giant cells multi-nuclear formation and a bone-resorbing efficiency reduction. Mice show increased bone mass. Older (>12 months) mice suffered from multisystemic inflammations in the kidney, lung and salivary gland. Mice show autoimmune symptoms, like dendritic cells (DC) with increased phagocytotic activity and antigen presentation.