IL‑4/IL‑4 Ab complex enhances the accumulation of both antigen‑specific and bystander CD8 T cells in mouse lungs infected with influenza A virus
10.1186/s42826-023-00183-2
- Author:
Hi Jung PARK
1
;
Eun Ah CHOI
;
Sung Min CHOI
;
Young‑Ki CHOI
;
Jae Il LEE
;
Kyeong Cheon JUNG
Author Information
1. Graduate Course of Translational Medicine, Seoul National University College of Medicine, Seoul 03080, Republic of Korea
- Publication Type:RESEARCH
- From:Laboratory Animal Research
2023;39(4):385-394
- CountryRepublic of Korea
- Language:English
-
Abstract:
Background:Unlike conventional T cells, innate and virtual-memory CD8 T cells in naïve mice acquire their memory phenotypes and functions in the absence of antigenic encounters in a cytokine-dependent manner. The relevant cytokines include interleukin-4 (IL-4), type I interferon, and interleukin-15 (IL-15). Moreover, exogenous IL-4 can also induce de novo generation and/or expansion of the virtual-memory CD8 T cell population. In this study, we investigated whether exogenous IL-4 could enhance the immune response to a viral infection.
Results:In vivo administration of IL-4 and an anti-IL-4 antibody complex (IL-4C) increased CXCR3 expression in both memory and naïve phenotype CD8 T cells in the absence of antigenic stimulation, and protected mice from lethal influenza infection. Flow cytometric analysis of lung-infiltrating immune cells on day 5 after virus infection revealed higher numbers of antigen-specific and bystander CD8 T cells in IL-4C-treated mice than in control mice. In particular, the bystander CD8 T cells were a naïve or evident memory phenotypes. Crucially, an anti-CXCR3 blocking antibody abrogated this IL-4C effect, reflecting that the increased accumulation of CD8 T cells in the lungs after IL-4C treatment is dependent on CXCR3.
Conclusions:These data demonstrate that exogenous IL-4C plays a protective role by enhancing CXCR3-dependent migration of CD8 T cells into influenza-infected lungs.
