Ifnlr1, known as interferon lambda receptor 1, is a type II cytokine receptor. It binds to interleukins IL-28A, IL-29B, and IL-29 (type III IFNs or IFN-λs). IFN-λs act via the JAK-STAT signaling pathway to exert antiviral effects, which are crucial for preventing and curing infections. Understanding its function is significant for comprehending immune responses and potential disease treatments [1,2,3,4,5].

In porcine alveolar macrophages (PAMs) infected with porcine reproductive and respiratory syndrome virus (PRRSV), overexpression of porcine IFNLR1 suppresses PRRSV replication, inhibits PAMs proliferation, and up-regulates antiviral and IFN-stimulated genes. In contrast, knockdown of IFNLR1 expression promotes PAMs proliferation [1]. In a TLR7-induced lupus model, Ifnlr1 deficiency significantly reduces immune cell activation and associated organ damage in the skin and kidneys without affecting autoantibody production [3]. In zebrafish, knockdown of ifnlr1 leads to a decrease in hair cells and non-inflation of the swim bladder, along with up-regulation of genes in the Jak1/STAT3 pathway [6].

In summary, Ifnlr1 plays a vital role in antiviral immunity, immune regulation, and is associated with certain diseases like PRRSV infection, lupus, and autosomal-dominant non-syndromic hearing loss. Studies using knockdown or knockout models in different species have revealed its functions in various biological processes, providing insights into potential therapeutic strategies for related diseases [1,3,6].