BioScience Trends. 2019;13(6):516-522. (DOI: 10.5582/bst.2019.01286)

IL16 deficiency enhances Th1 and cytotoxic T lymphocyte response against influenza A virus infection.

Jia R, Liu S, Xu J, Liang XZ


Influenza A virus (IAV) is the major cause of seasonal epidemics and flu outbreaks worldwide. Given that interleukin 16 (IL16) can regulate T cell function and is one of the signature markers for virus infection including IAV infection, the impact of IL16 on IAV-induced T cell immune response hasn’t been elucidated yet. In this paper, we infected wild type and IL16 knockout (KO) mice with IAV and analyzed the immunity of mice by flow cytometry. We observed an increase in the percentage of T helper (Th) 1 cells in the spleens of IL16 KO mice and elevation of IFN-γ and TNF-ɑ secretion from CD8+ T cells in the lungs and spleens of IL16 KO mice in response to IAV infection. Moreover, the expression of major histocompatibility complex II which represents the maturation of dendritic cells (DCs) was upregulated in the lungs of IL16 KO mice. Taken together, our study suggests that IL16 deficiency enhanced Th1 and cytotoxic T lymphocyte response as well as DC maturation upon IAV infection, which provides new insight into the host regulation of T cell immune responses during IAV infection.

KEYWORDS: Interleukin 16, influenza A virus, T helper 1, cytotoxic T lymphocyte

Full Text: