Sialoadhesin (SIGLEC-1) is a cell adhesion molecule found on the surface of various immune cells. It is found in especially high amounts on macrophages of the spleen, liver, lymph node, bone marrow, colon, and lungs.
Sialoadhesin binds to certain molecules called sialic acids. During this binding process a salt bridge is formed between a highly conserved arginine residue (in the V-set domain) and the carboxylate group of the sialic acid.[7] Since sialoadhesin binds sialic acids with its N-terminal IgV-domain, it is also a member of the Siglec family. Alternate names for sialoadhesin include siglec-1 and CD169 (cluster of differentiation 169).[8]
Sialoadhesin (CD169) positive macrophages, along with mesenchymal stem cells and beta-adrenergic neurons, form the hematopoietic stem cell niche in the bone marrow. CD169+ macrophages mediate signaling between the various cells and seem to promote hematopoietic stem cell retention to the niche.
Siglec-1 is also expressed on lymph node subcapsular sinus macrophages. Research using a murine melanoma model has demonstrated that these subcapsular sinus macrophages bind to sialylated proteins present on the surface of pioneer metastatic cells shortly after their landing in the lymph nodes. This interaction serves as a critical step in metastatic colonization, providing a conducive environment, or 'soil,' for the establishment and proliferation of pioneer metastatic cells, often referred to as 'seeds.'[10]
^Varki A (2001-09-10). "Sialoadhesin, Siglec-1 (CD169)". Protein Reviews on the Web (PROW) Guide. United States National Center for Biotechnology Information (NCBI). Archived from the original on 2007-07-01. Retrieved 2011-04-15.
^Kelm S, Pelz A, Schauer R, Filbin M, Tang S, de Bellard M, et al. (1994). "Sialoadhesin, myelin-associated glycoprotein and CD22 define a new family of sialic acid-dependent adhesion molecules of the immunoglobulin superfamily". Current Biology. 4 (11): 965–972. Bibcode:1994CBio....4..965K. doi:10.1016/S0960-9822(00)00220-7. PMID7533044. S2CID20282803.
