tetano
Editor, Senior Moderator
Lab Anim Res
. 2023 Dec 1;39(1):32.
doi: 10.1186/s42826-023-00183-2. 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
Hi Jung Park[SUP] 1 [/SUP], Eun Ah Choi[SUP] 1 [/SUP], Sung Min Choi[SUP] 1 [/SUP], Young-Ki Choi[SUP] 2 [/SUP], Jae Il Lee[SUP] 3 4 5 [/SUP], Kyeong Cheon Jung[SUP] 6 7 8 9 [/SUP]
Affiliations
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.
Keywords: CD8 T cells; CXCR3; Influenza; Interlukin-4; Virtual memory.
. 2023 Dec 1;39(1):32.
doi: 10.1186/s42826-023-00183-2. 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
Hi Jung Park[SUP] 1 [/SUP], Eun Ah Choi[SUP] 1 [/SUP], Sung Min Choi[SUP] 1 [/SUP], Young-Ki Choi[SUP] 2 [/SUP], Jae Il Lee[SUP] 3 4 5 [/SUP], Kyeong Cheon Jung[SUP] 6 7 8 9 [/SUP]
Affiliations
- PMID: 38037190
- DOI: 10.1186/s42826-023-00183-2
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.
Keywords: CD8 T cells; CXCR3; Influenza; Interlukin-4; Virtual memory.