CD55 is a glycoprotein that is broadly distributed among hematopoietic and non-hematopoietic cells. It is a 70-75 kDa membrane protein that attaches to the cell membrane via a glycophosphatidylinositol (GPI) anchor . The protein contains four complement control protein (CCP) repeats, which are involved in its inhibition of the complement pathways. Specifically, CCP2 and CCP3 are involved in the inhibition of the classical pathway, while CCP2, CCP3, and CCP4, along with three consecutive lysine residues in a positively charged pocket between CCP2 and CCP3, are involved in the inhibition of the alternate complement pathway .
CD55 regulates the complement system by recognizing C4b and C3b fragments that are created during the activation of C4 (classical or lectin pathway) or C3 (alternative pathway). Interaction of CD55 with cell-associated C4b interferes with the conversion of C2 to C2b, thereby preventing the formation of the C4b2a C3-convertase. Similarly, interaction of CD55 with C3b interferes with the conversion of factor B to Bb by factor D, thereby preventing the formation of the C3bBb C3 convertase of the alternative pathway . By limiting the amplification convertases of the complement cascade, CD55 indirectly blocks the formation of the membrane attack complex.
Recombinant mouse CD55 is produced using a mouse myeloma cell line, NS0-derived mouse CD55/DAF protein. The recombinant protein is typically purified to a high degree of purity, often greater than 90%, as determined by SDS-PAGE under reducing conditions and visualized by silver stain . The recombinant protein is often used in various research applications, including functional assays and binding studies.
Recombinant mouse CD55 has been used in various research areas, including studies on immune evasion by pathogens, granulocyte homeostasis, and anti-inflammatory responses . For example, CD55 has been shown to facilitate immune evasion by certain pathogens, such as Borrelia crocidurae, the causative agent of relapsing fever . Additionally, CD55 is a ligand of the adhesion class G protein-coupled receptor CD97, and this interaction has been studied in the context of granulocyte homeostasis .
CD55 is also implicated in certain pathological conditions. For instance, in paroxysmal nocturnal hemoglobinuria (PNH), a disorder characterized by complement-mediated hemolysis, the expression of CD55 is reduced due to mutations that affect GPI anchor synthesis . This reduction in CD55 expression leads to increased susceptibility of red blood cells to complement-mediated lysis, resulting in symptoms such as anemia, fatigue, and episodes of dark-colored urine.