In Paroxysmal nocturnal hemoglobinuria, RBCs have deficiency of which surface proteins?

In Paroxysmal nocturnal hemoglobinuria, RBCs have deficiency of which surface proteins?

• A. CD55
• B. CD59
• C. CD55 and CD59
• D. CD14

Answer: (D)

Paroxysmal nocturnal hemoglobinuria arises from a defect in the GPI anchor that attaches certain proteins to the cell surface. Red blood cells deficient in GPI anchors lose two key protective proteins: CD55 (Decay-accelerating Factor) and CD59 (protectin). CD55 normally accelerates the decay of C3/C5 convertases, limiting complement activation, while CD59 prevents formation of the membrane attack complex. Without these regulators, RBCs become highly susceptible to complement-mediated lysis, leading to intravascular hemolysis, especially at night when mild acidosis can promote complement activity. CD14 is not a primary issue here; it is a monocyte/macrophage marker and not a major regulator of RBC surface protection. So the proteins deficient on RBCs in PNH are CD55 and CD59.

Paroxysmal nocturnal hemoglobinuria arises from a defect in the GPI anchor that attaches certain proteins to the cell surface. Red blood cells deficient in GPI anchors lose two key protective proteins: CD55 (Decay-accelerating Factor) and CD59 (protectin). CD55 normally accelerates the decay of C3/C5 convertases, limiting complement activation, while CD59 prevents formation of the membrane attack complex. Without these regulators, RBCs become highly susceptible to complement-mediated lysis, leading to intravascular hemolysis, especially at night when mild acidosis can promote complement activity. CD14 is not a primary issue here; it is a monocyte/macrophage marker and not a major regulator of RBC surface protection. So the proteins deficient on RBCs in PNH are CD55 and CD59.