Interferon Lambda 1 (IFNL1), a member of the type III interferon (IFN-λ) family, plays a critical role in innate immunity by inducing antiviral responses, particularly at mucosal surfaces. It signals through a heterodimeric receptor complex (IFNLR1/IL10R2) to activate JAK-STAT pathways, leading to the expression of interferon-stimulated genes (ISGs) that inhibit viral replication. IFNL1 is primarily produced by epithelial cells and certain immune cells in response to viral infections, such as hepatitis C virus (HCV) or influenza.
Antibodies targeting IFNL1 are valuable tools for studying its biological functions and therapeutic potential. Research-grade anti-IFNL1 antibodies enable detection, quantification, and neutralization of IFNL1 in experimental models, aiding investigations into its role in viral clearance, inflammation, and immune regulation. Clinically, IFNL1 has been linked to chronic liver diseases, and its genetic variants (e.g., near IFNL3) influence treatment outcomes in HCV. Neutralizing antibodies may help explore IFNL1's dual roles in promoting antiviral defense versus contributing to pathological inflammation.
Current studies also explore IFNL1 antibodies in autoimmune disorders and cancer, where dysregulated IFN-λ signaling may drive disease progression. However, therapeutic applications remain exploratory, with challenges in balancing antiviral efficacy and inflammatory side effects. Overall, IFNL1 antibodies serve as both research reagents and potential candidates for modulating IFN-λ pathways in disease contexts.