Which cell surface marker is deficient in paroxysmal nocturnal hemoglobinuria?

In paroxysmal nocturnal hemoglobinuria (PNH), there is a deficiency of specific cell surface markers due to mutations in the PIGA gene, which leads to a lack of glycosylphosphatidylinositol (GPI)-anchored proteins. CD55, also known as decay-accelerating factor (DAF), is one of these GPI-anchored proteins. Its primary role is to regulate the complement system and prevent complement-mediated lysis of red blood cells.

In patients with PNH, the absence of CD55 on the surface of erythrocytes renders them susceptible to uncontrolled complement activation, resulting in hemolysis and the release of hemoglobin into the urine, which is characteristic of the condition. This lack of protective factors on the cell surface is fundamental to understanding the pathology of PNH, as it highlights the immunological mechanisms that lead to the anemia and associated symptoms seen in affected individuals.

In contrast, the other markers listed do not have the same direct association with PNH. CD16, CD45, and CD95 are not GPI-anchored proteins and are not deficient in this specific hematological disorder. Their roles are related to other immune functions or cell signaling pathways, making