Ifnl2, also known as IL28A, is a member of the type III interferon (IFN) gene family. Type III IFNs are important components of the innate immune response, especially in mucosal antiviral defense [3,4,5,6]. They are involved in various cellular functions, including regulation of the Jak-STAT pathway [6]. Ifnl2, like other type III IFNs, is thought to play a crucial role in the body's response to viral infections and may be involved in regulating innate immune responses [2,5]. Genetic models, such as gene knockout mouse models, are valuable tools for studying Ifnl2.

Disruption of Ifnl2 and Ifnl3 genes in mice recapitulates the loss of the type III IFN receptor in the mucosal antiviral response. Ifnl2 -/- Ifnl3 -/- mice display defective control of murine norovirus, reovirus, and influenza virus, similar to Ifnlr1 -/- mice lacking IFNLR signaling, indicating that Ifnl2 and Ifnl3 are essential for regulating viral infections at mucosal sites of the intestine and lung [3]. In HepG2 cells, a new transcription factor ATG10S promotes Ifnl2 gene transcription by competing with IRF1 for the same binding site [1]. Also, hepatitis C virus-induced microRNAs can suppress Ifnl2 expression, which may support viral persistence [4].

In conclusion, Ifnl2 is an essential part of the mucosal antiviral innate immune response. The study of Ifnl2 knockout mouse models has revealed its significance in controlling mucosal viral infections. Additionally, understanding its transcriptional regulation and the factors influencing its expression, as shown in cell-based studies, contribute to our knowledge of how the body responds to viral infections, particularly in the context of hepatitis C virus infection [1,3,4].