Abstract Despite the success of the pneumococcal conjugate vaccine, pneumococcal pneumonia remains a significant clinical problem, and there is still much to learn about natural resistance and cellular immunity to pneumococcus. We investigated the role of T lymphocytes in resistance to serotype (ST) 3 Streptococcus pneumoniae in an intranasal infection model in C57BL/6 (wild-type [Wt]) and CD8+ (CD8−/−)- and CD4+ (MHC class II−/−)-deficient mice. CD8−/− mice exhibited significantly more bacterial dissemination and lung inflammation and a significantly more lethal phenotype than Wt mice. However, there was no difference in the bacterial dissemination, lung inflammation, or survival of Wt and MHC class II−/− mice. Perforin (Pfn)−/− and IFN-γ−/− mice, which were used to dissect the role of CD8+ T cells in our model, also exhibited a more lethal survival phenotype than Wt mice. Comparison of lung chemokine/cytokine levels by Luminex and cellular recruitment by FACS in Wt mice and knockout strains revealed that CD8−/− and IFN-γ−/− mice, which had the most lethal survival phenotype, had more CD4+IL-17+ T (Th17) cells, IL-17, neutrophil chemoattractants, and lung neutrophils, and fewer regulatory T cells than Wt mice. CD4+ T cell depletion improved the survival of ST-infected CD8−/− mice, and survival studies in Th17-deficient mice revealed that the Th17 response was dispensable for ST3 resistance in our model. Taken together, these findings demonstrate that CD8+ cells are required, but CD4+ T cells are dispensable for resistance to ST3 pneumonia in mice and suggest a previously unsuspected role for CD8+ cells in modulating the inflammatory response to ST3.