ITGAE Knockout Cell Line (HEK 293)

The choice depends on whether you are studying ITGAE (CD103, integrin αE)'s role as the principal intraepithelial lymphocyte integrin or its functions in tissue-resident memory T cell (Trm) biology and cancer immunology. The Knockout line is the standard tool for asking whether ITGAE is required for these processes — ITGAE partners exclusively with ITGB7 to form αEβ7 (CD103), which binds E-cadherin on epithelial cells, mediating intraepithelial lymphocyte retention in mucosal tissues and Trm establishment. Overexpression is useful for studying ITGAE in heterologous expression contexts. For tumor immunology research, the EDITGENE ITGAE Knockout in HEK293 enables study of CD103 biology — CD103+ tissue-resident memory T cells are key effectors in anti-tumor immunity and predict immune checkpoint inhibitor response in multiple cancers. Rescue with wild-type or E-cadherin-binding-deficient ITGAE is the standard specificity control. The knockout is valuable for studying Trm cell biology, dendritic cell subsets (CD103+ DCs are critical for tumor antigen cross-presentation), and emerging CD103-targeted immunotherapy strategies.

Primary applications: • E-cadherin binding: αEβ7-E-cadherin binding analysis in heterologous epithelial co-culture systems. • Trm cell biology: in heterologous T cell-relevant contexts, characterization of CD103-dependent tissue-resident memory T cell biology. • CD103+ DC studies: in dendritic cell-relevant contexts, characterization of CD103-dependent dendritic cell tumor antigen cross-presentation. • Immune checkpoint inhibitor biomarker: CD103+ Trm cells correlate with immune checkpoint inhibitor response — CD103 KO enables mechanism studies. EDITGENE recommends this model for researchers investigating CD103 biology, tissue-resident memory T cell mechanisms, and CD103-targeted cancer immunotherapeutic strategies.

Yes. ITGAE rescue experiments require attention to αEβ7 heterodimer formation: • Construct design: use a codon-modified ITGAE sequence with a small intracellular C-terminal tag (FLAG, HA). ITGAE has the canonical α-integrin architecture with β-propeller and I domain — preserve all elements. • Surface localization validation: confirm αEβ7 heterodimer surface expression before functional assays. • E-cadherin-binding-deficient rescue: I domain MIDAS site mutations abolish E-cadherin binding and serve as the standard specificity control. • ITGB7 partnership: ITGAE requires ITGB7 for surface expression — rescue interpretation considers β7 levels. • Functional readout: rescue should restore αEβ7-dependent binding to E-cadherin-expressing epithelial cells. HEK293 transduces efficiently with lentivirus and supports stable rescue line generation.