Human CLEC7A Stable Cell Line - BEAS-2B

The CLEC7A gene (Dectin-1) encodes a non-canonical C-type lectin receptor, crucial for detecting β-glucan, a structural carbohydrate found in fungi, bacteria, and plants. Dectin-1 is highly expressed on the surface of phagocytes but is also present in some epithelial cell populations. Structurally, the receptor consists of an extracellular C-type lectin domain (CTLD) and an intracellular tail containing a tyrosine signaling motif called a hemi-ITAM. Activation of Dectin-1 is essential for inducing Th17 immune responses, which are crucial for mucosal defense against extracellular pathogens. Recent studies have also highlighted the role of Dectin-1 in sensing endogenous ligands released from damaged tissue (damage-associated molecular patterns, DAMPs), suggesting its involvement in aseptic inflammation and tissue repair. Clinically, variations in the CLEC7A gene are associated with the severity of inflammatory bowel disease (IBD) and the risk of certain occupational lung diseases following exposure to environmental dust and mold.

BEAS-2B cells are human bronchial epithelial cells with a normal karyotype, commonly used to study the mechanisms of asthma and environmental exposure. This cell line provides a stable platform for the expression of human CLEC7A, enabling researchers to assess how the perception of β-glucan by airway epithelial cells leads to asthma exacerbations and Th17 cell recruitment. This product is particularly suitable for screening Dectin-1 antagonists or antibodies designed to limit excessive inflammatory responses in fungal-induced respiratory diseases. The CLEC7A-BEAS-2B model is also a powerful platform for studying the synergistic effects of Dectin-1 ligands in combination with conventional bronchodilators or corticosteroids. The stability of this cell line ensures highly reproducible analysis of the molecular mechanisms of Syk-mediated signaling pathways and allows for validation across multiple generations.