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-γ 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-γ and IL-17 from these cells back to basal levels. The reduction in IL-2 secretion is not seen in IFN-γ^−/− and iNOS^−/− mice infected with Salmonella. Our findings demonstrate that sustained innate activated IFN-γ 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.

致病性 沙门氏菌血清型是人类和动物肠道疾病的主要原因，并产生从局部性肠胃炎到全身性疾病的临床表现。T细胞是抵抗这种细胞内病原体的免疫力的重要组成部分。该机制沙门氏菌调节T细胞介导的免疫反应以建立全身性感染尚不完全清楚。我们证明感染的小鼠肠沙门氏菌 鼠伤寒血清小号。鼠伤寒（Typhimurium）可抑制IL-2并增加活化T细胞产生的IFN-γ和IL-17体内 要么 离体通过T细胞受体。感染小号。鼠伤寒导致CD11b ⁺ Gr1 ⁺抑制细胞募集到脾脏。离体这些细胞的耗尽恢复了活化的T细胞产生IL-2的能力，并使这些细胞的IFN-γ和IL-17分泌恢复至基础水平。在感染了IFN-γ ^-/-和iNOS ^-/-的小鼠中未观察到IL-2分泌的减少沙门氏菌。我们的发现表明，在感染的过程中持续的先天活化的IFN-γ产生沙门氏菌 通过iNOS介导的信号传导途径降低T细胞的IL-2分泌能力，这可能会对这种病原体的长期免疫产生不利影响。