| First Author | Yadav J | Year | 2020 |
| Journal | Front Immunol | Volume | 11 |
| Pages | 514 | PubMed ID | 32269573 |
| Mgi Jnum | J:312579 | Mgi Id | MGI:6728964 |
| Doi | 10.3389/fimmu.2020.00514 | Citation | Yadav J, et al. (2020) Innate Activation of IFN-gamma-iNOS Axis During Infection With Salmonella Represses the Ability of T Cells to Produce IL-2. Front Immunol 11:514 |
| abstractText | Pathogenic Salmonella serovars are a major cause of enteric illness in humans and animals, and produce clinical manifestations ranging from localized gastroenteritis to systemic disease. T cells are a critical component of immunity against this intracellular pathogen. The mechanisms by which Salmonella modulates T-cell-mediated immune responses in order to establish systemic infection are not completely understood. We show that infection of mice with Salmonella enterica serovar Typhimurium (S. Typhimurium) suppresses IL-2 and increases IFN-gamma and IL-17 production from T cells activated in vivo or ex vivo through the T cell receptor. Infection with S. Typhimurium brings about recruitment of CD11b(+)Gr1(+) suppressor cells to the spleen. Ex vivo depletion of these cells restores the ability of activated T cells to produce IL-2 and brings secretion of IFN-gamma and IL-17 from these cells back to basal levels. The reduction in IL-2 secretion is not seen in IFN-gamma(-/-) and iNOS(-/-) mice infected with Salmonella. Our findings demonstrate that sustained innate activated IFN-gamma production during progression of infection with Salmonella reduces IL-2-secreting capability of T cells through an iNOS-mediated signaling pathway that can adversely affect long term immunity against this pathogen. |
