| First Author | Lee Y | Year | 2019 |
| Journal | Front Immunol | Volume | 10 |
| Pages | 1172 | PubMed ID | 31244826 |
| Mgi Jnum | J:281446 | Mgi Id | MGI:6377823 |
| Doi | 10.3389/fimmu.2019.01172 | Citation | Lee Y, et al. (2019) Interleukin-17D Promotes Pathogenicity During Infection by Suppressing CD8 T Cell Activity. Front Immunol 10:1172 |
| abstractText | Interleukin-17D (IL-17D) belongs to the IL-17 family of cytokines. While the members of the IL-17 family have been implicated in inflammation and host defense, the function of IL-17D remains unclear. Here, we showed that the lack of IL-17D expression confers protection against Listeria infection. A deficiency in IL-17D also resulted in less weight loss with reduced pathogen burden during influenza A virus infection. During infection, the loss of IL-17D resulted in compromised CD8 T cell activity. CD8 T cell depletion in IL-17D-deficient mice restored the bacterial burden to a level similar to that found in WT mice. Similarly, IL-17D-deficient mice in a RAG-deficient background had no difference in bacterial and viral burden compared to WT mice. IL-17D controlled CD8 T cell activity in part by suppressing the function of dendritic cells. We found that IL-17D from the non-hematopoietic compartment regulates protective immunity during infection. Together, our data led to the identification of IL-17D as a critical cytokine during intracellular bacteria and virus infection that suppresses the activity of CD8 T cells by regulating dendritic cells. |
