The CD55 Knockout HeLa Polyclonal Cells are a CRISPR/Cas9-edited polyclonal knockout cell population derived from the HeLa cell line, featuring targeted disruption of the CD55 gene. This product provides a heterogeneous pool of knockout cells, allowing researchers to study loss-of-function phenotypes in a well-characterized epithelial carcinoma background. As a polyclonal population, it captures diverse genetic modification profiles, making it suitable for experiments where clonal effects are minimal or bulk population responses are desired.
HeLa cells, an immortalized cervical epithelial adenocarcinoma line originally isolated from a patient with HPV18 infection, are widely used in biomedical research for studying epithelial cell biology, cancer progression, and host-pathogen interactions. Their robust growth characteristics and extensive characterization make them an ideal host for investigating complement regulatory mechanisms and tumor immune evasion strategies. The epithelial origin of HeLa cells provides a relevant context for assessing CD55 function in carcinomas, where complement resistance contributes to tumor survival.
CD55 encodes a glycosylphosphatidylinositol (GPI)-anchored membrane protein that inhibits complement activation by accelerating the decay of C3 and C5 convertases, preventing formation of the membrane attack complex (C5b-9). Its expression is upregulated by inflammatory cytokines TNF-alpha, IL-1, and IFN-gamma, and transcription factors SP1 and NF-kB, with additional induction under hypoxia. CD55 interacts with C3b, C4b, CD97, and CD59, and its activity suppresses C5b-9 deposition, complement-dependent cytotoxicity, and pro-inflammatory cytokine release. Knockout disrupts these protective interactions, sensitizing cells to complement-mediated lysis. In the complement cascade, CD55 acts on C3 convertase (C3b, Factor B, Factor D) and C5 convertase, with properdin stabilization, ultimately blocking the lytic pore.
In HeLa cells, CD55 knockout eliminates a key immune evasion mechanism, sensitizing them to complement-mediated lysis and inflammatory responses. This model is particularly relevant for paroxysmal nocturnal hemoglobinuria (PNH) research, where CD55 deficiency leads to hemolysis, and for studying tumor survival strategies in HPV18-positive cervical carcinoma. It enables investigation of how complement resistance supports cancer cell viability and immune escape.
Research applications include complement regulation studies, cancer immune evasion, drug screening for complement inhibitors, echovirus infection mechanisms (CD55 is a receptor), and GPI-anchor biology. Representative assays for knockout validation and functional analysis encompass Western blotting for CD55, flow cytometry for surface CD55, complement-dependent cytotoxicity assay, C3b deposition assay, immunofluorescence for C5b-9, and RT-qPCR for CD55 mRNA. These tools enable detailed characterization of complement dynamics and therapeutic evaluation. For further information, please contact Ascent Research.
