Il16, also known as interleukin 16, is a pro-inflammatory cytokine. It is synthesized as a precursor and processed into bioactive tetramers. IL16 functions through interaction with CD4, and is involved in processes such as chemotaxis induction, regulation of immune cell activation, and is associated with multiple biological pathways related to inflammation and immune responses [3,4].

In an in vivo study, IL16 knockout (KO) mice infected with Influenza A virus (IAV) showed an increase in the percentage of Th1 cells in the spleen and elevation of IFN-γ and TNF-α secretion from CD8+ T cells in the lungs and spleens, along with upregulated major histocompatibility complex II in the lungs, suggesting that IL16 deficiency enhances Th1 and cytotoxic T lymphocyte response as well as dendritic cell maturation upon IAV infection [2]. In a rat model of osteoarthritis (OA), IL16 was upregulated. Knockdown of IL16 downregulated the expression of MMP3 and MMP13, suggesting its role in OA progression [1].

In conclusion, Il16 plays a crucial role in regulating immune responses and inflammation. The study of Il16 KO mouse models has provided insights into its role in viral infection-related immune responses and OA progression, highlighting its importance in understanding these disease mechanisms.