Which complement receptor is specifically implicated in paroxysmal nocturnal hemoglobinuria (PNH)?

In paroxysmal nocturnal hemoglobinuria (PNH), the complement receptors CD 55 and CD 59 play a crucial role. PNH is a disorder characterized by the destruction of red blood cells due to complement-mediated lysis.

In healthy individuals, CD 55 (also known as decay-accelerating factor) functions to regulate the complement system by preventing the formation and stabilization of the C3 and C5 convertases, thus inhibiting the complement cascade that leads to cell lysis. CD 59, on the other hand, inhibits the formation of the membrane attack complex (MAC), which is the component of the complement system that causes cell lysis.

In patients with PNH, mutations in the PIGA gene lead to the absence of glycosylphosphatidylinositol (GPI) anchors that are necessary for the expression of CD 55 and CD 59 on the surface of red blood cells. Without these protective proteins, red blood cells become susceptible to lysis by the complement system, leading to the characteristic hemolytic anemia seen in PNH. This highlights the critical function of CD 55 and CD 59 in protecting red blood cells from complement-mediated destruction, making them specifically implicated in the