Final answer:
Red blood cells without GPI anchors are prone to complement-mediated lysis because they lack protective proteins that prevent complement activation. This leads to their destruction in conditions like mismatched transfusions or erythroblastosis fetalis, causing hemolytic anemia and potential jaundice.
Step-by-step explanation:
Red blood cells (RBCs) that lack glycosylphosphatidylinositol (GPI) anchors on their surface are vulnerable to complement-mediated lysis due to the absence of key protective proteins. GPI anchors are used to attach various proteins, including those that regulate complement activation, to the cell membrane.
Without GPI anchors, protective elements like CD55 and CD59, which normally prevent the formation of the membrane attack complex (MAC) of the complement system, cannot anchor to the cell surface. As a result, RBCs become susceptible to the unrestricted action of the complement system, leading to their destruction.
During events like a transfusion of mismatched blood type or erythroblastosis fetalis, antibodies bind to RBC antigens, triggering the complement system. This response is a type of type II hypersensitivity, where cell damage is principally due to complement activation and antibody binding. The destruction of RBCs by the complement system results in the release of hemoglobin, which, when in solution, can visually indicate hemolysis due to the pink coloration.
Lastly, the energy requirement and metabolism of RBCs are also tied to GPI-anchored enzymes. Red blood cells rely on glycolysis for energy, and a deficiency in this process can cause membrane injury and lead to their lysis. The lysis of RBCs contributes to hemolytic anemia and can significantly affect tissue oxygenation and cause jaundice due to increased plasma bilirubin.