Acts as a cofactor for complement factor I, a serine protease which protects autologous cells against complement-mediated injury by cleaving C3b and C4b deposited on host tissue. May be involved in the fusion of the spermatozoa with the oocyte during fertilization. Also acts as a costimulatory factor for T-cells which induces the differentiation of CD4+ into T-regulatory 1 cells. T-regulatory 1 cells suppress immune responses by secreting interleukin-10, and therefore are thought to prevent autoimmunity.
(Microbial infection) A number of viral and bacterial pathogens seem to bind MCP in order to exploit its immune regulation property and directly induce an immunosuppressive phenotype in T-cells.
(Microbial infection) Acts as a receptor for Adenovirus subgroup B2 and Ad3.
(Microbial infection) Acts as a receptor for cultured Measles virus.
(Microbial infection) Acts as a receptor for Herpesvirus 6/HHV-6.
(Microbial infection) May act as a receptor for pathogenic bacteria Neisseria and Streptococcus pyogenes ( , ).
Subcellular locations: Cytoplasmic vesicle, Secretory vesicle, Acrosome inner membrane
Inner acrosomal membrane of spermatozoa. Internalized upon binding of Measles virus, Herpesvirus 6 or Neisseria gonorrhoeae, which results in an increased susceptibility of infected cells to complement-mediated injury. In cancer cells or cells infected by Neisseria, shedding leads to a soluble peptide.
Expressed by all cells except erythrocytes.