The FLG2 Knockout Raji Polyclonal Cells are a CRISPR/Cas9-edited polyclonal population of Raji B lymphocytes, where the FLG2 gene has been disrupted to establish a loss-of-function model. This polyclonal pool, free from clonal selection bias, retains parental Raji characteristics while enabling robust investigation of FLG2-related signaling and immune interactions.
The Raji cell line, derived from Burkitt lymphoma, is a suspension-adapted B lymphocyte model frequently used in immunology and cancer research. It expresses B cell markers and is permissive to EBV infection, facilitating studies of lymphomagenesis and antiviral responses. Knocking out FLG2 in this background provides a novel system to examine non-epidermal filaggrin functions in lymphocytes.
FLG2 encodes a filaggrin family protein critical for epidermal barrier maintenance by mediating keratin filament aggregation and cornified envelope formation. Its expression is regulated by p63, AP-1 (c-Fos/c-Jun) and Notch1 signaling. FLG2 protein interacts with loricrin, involucrin, and small proline-rich proteins to strengthen the cornified envelope. Downstream, it modulates the release of alarmins TSLP and IL-33, which drive type 2 inflammation upon barrier breach. Within the keratinization pathway, FLG2 functions alongside KRT1, KRT10, loricrin, involucrin, transglutaminase 1 (TGM1), and filaggrin (FLG), forming an integrated network essential for epidermal differentiation.
Disrupting FLG2 in Raji B lymphocytes enables exploration of filaggrin signaling beyond its conventional epidermal role, allowing interrogation of crosstalk with B cell receptor pathways, cytokine networks, or EBV latency programs. This model is relevant for understanding how filaggrin gene alterations impact immune surveillance and inflammatory processes in diseases such as atopic dermatitis, ichthyosis vulgaris, and psoriasis.
This polyclonal knockout pool supports functional studies of FLG2 in B lymphocytes, high-throughput drug screening for barrier restoration, and investigation of filaggrin-related immune mechanisms involving TSLP/IL-33. Genomic editing can be verified by Sanger sequencing, while gene expression is assessed via RT-qPCR and RNA-seq. Protein analysis employs Western blotting and immunofluorescence, with cytokine secretion profiled by ELISA. These methods collectively enable thorough characterization of FLG2 loss-of-function in hematopoietic cells. For further information, please contact Ascent Research.
