The CD55 Knockout K-562 Polyclonal Cells constitute a CRISPR/Cas9-edited polyclonal knockout population derived from the K-562 cell line, with targeted disruption of the CD55 gene encoding decay accelerating factor (DAF). This polyclonal format provides a heterogeneous pool of knockout cells, enabling broad functional assessment of complement regulation without clonal selection artifacts.
The parental K-562 line was established from the pleural effusion of a 53-year-old female with chronic myelogenous leukemia in blast crisis and represents a widely used lymphoblast model for hematopoietic differentiation, leukemia biology, and innate immune research.
CD55 is a glycosylphosphatidylinositol-anchored membrane protein that regulates the complement cascade by accelerating the decay of C3 and C5 convertases, thereby limiting C3b and C4b deposition and preventing assembly of the C5b-9 membrane attack complex. Its expression is modulated by inflammatory cytokines such as TNF-?? and IL-1??, and it interacts directly with C3b, C4b, CD97, and certain enteroviruses. In the absence of CD55, complement activation proceeds unchecked, leading to enhanced opsonization and complement-dependent cytotoxicity.
K-562 cells naturally express CD55, contributing to their resistance to complement-mediated lysis. Disruption of CD55 in this lymphoblast background creates a powerful tool to dissect complement regulatory mechanisms, model paroxysmal nocturnal hemoglobinuria (PNH)-like phenotypes, and investigate immune evasion strategies employed by leukemic cells. The polyclonal nature of the knockout population preserves diverse mutations, enabling robust functional characterization of complement susceptibility without clonal bias.
This CD55 knockout polyclonal cell product is ideally suited for complement-dependent cytotoxicity assays, flow cytometric quantification of surface CD55 and C3/C4 opsonization, RT-qPCR and western blot validation of CD55 loss, and apoptosis or viability assessments following serum or purified complement exposure. Researchers studying hematological malignancies, complement dysregulation disorders, autoimmune hemolytic anemia, and therapeutic complement inhibitors will find this model invaluable. For further information, please contact Ascent Research.
