CD55 is a membrane-bound complement regulatory protein that functions as a critical negative regulator of complement activation. Structurally, CD55 regulates complement by inhibiting both the C3 and C5 convertases 1. Additionally, CD55 serves as a receptor for human echoviruses 6, 7, 11, 12, 20, and 21, facilitating viral entry. CD55's primary disease relevance involves complement-mediated hemolytic disorders. In paroxysmal nocturnal hemoglobinuria (PNH), loss of CD55 expression due to PIGA gene mutations prevents the cell-surface presence of this complement regulator, rendering red blood cells susceptible to complement-mediated hemolysis and thrombosis 2. CD55 deficiency increases susceptibility to hemolytic anemia through uncontrolled complement activation 3. In cancer pathology, CD55 plays contradictory roles. In lung cancer, elevated CD55 expression suppresses complement system activation and CD8+ T cell responses, promoting tumor immune evasion and checkpoint blockade resistance 4. In ovarian cancer, nuclear-localized CD55 drives platinum chemoresistance and cancer stem cell maintenance through PRC2-mediated H3K27 trimethylation 5. CD55 expression is regulated by transcription factors (TFCP2, NF-κB) and miR-27a-3p in colon cancer 6. Clinically, CD55 manipulation shows therapeutic potential: complement inhibitor therapy benefits PNH patients 2, increased CD55 expression protects against renal ischemia-reperfusion injury 1, and blocking CD55 nuclear entry represents a strategy for overcoming platinum resistance in ovarian cancer 5. In pregnancy, decreased CD55 expression associates with miscarriage and infertility 7.