CD59 is a GPI‑anchored complement regulatory protein on blood cell membranes that prevents formation of the membrane attack complex (C5b–C9). In PNH, PIGA mutations cause loss of CD59 from red cells and other blood cells, permitting unchecked complement‑mediated intravascular hemolysis and increased thrombosis risk. Flow cytometry detects CD59 deficiency for diagnosis and guides complement‑inhibitor therapy.

PNH is marked by loss of GPI-anchored proteins—particularly CD55 and CD59—on red cells and leukocytes, detected by flow cytometry (often using FLAER). Laboratory markers include intravascular hemolysis (hemoglobinuria, elevated LDH, low haptoglobin, indirect hyperbilirubinemia, reticulocytosis), cytopenias, and an increased tendency for thrombosis. Historic tests include sucrose lysis or Ham test, but flow cytometry is diagnostic.

CD55 (decay-accelerating factor) and CD59 (protectin) are membrane proteins that protect host cells from complement-mediated damage. CD55 disrupts formation and accelerates decay of C3/C5 convertases, limiting complement activation. CD59 prevents membrane attack complex formation by blocking C9 polymerization, avoiding cell lysis. Both are broadly expressed on blood cells and endothelium; loss increases complement-driven injury.

The gold standard test for paroxysmal nocturnal hemoglobinuria (PNH) is flow cytometry demonstrating deficiency of GPI‑anchored proteins on blood cells. Multiparameter flow cytometry uses antibodies to CD55 and CD59 and FLAER (which binds GPI anchors) on red cells, granulocytes, and monocytes to detect and quantify PNH clones with high sensitivity and specificity.

The hallmark of paroxysmal nocturnal hemoglobinuria is complement‑mediated intravascular hemolysis from acquired loss of GPI‑anchored complement regulators (CD55 and CD59) on red cells. This causes episodic hemoglobinuria—often darker in the morning—variable anemia, high thrombosis risk, and potential bone marrow failure. Diagnosis relies on flow cytometry demonstrating loss of these proteins on blood cells.

CD59 is also called protectin or MAC-inhibitory protein (MAC-IP). It is a small GPI‑anchored membrane glycoprotein that protects host cells by preventing formation of the membrane attack complex of complement. Also referred to as the CD59 antigen or CD59 glycoprotein, it helps prevent complement-mediated cell lysis and modulates immune responses.