Klebsiella pneumoniae (Kp) is a versatile pathogen capable of causing numerous infections that are becoming increasingly difficult to treat due to increasing antibiotic resistance. Kp strains are categorized into two distinct pathotypes: classical and hypervirulent, which exhibit critical differences in pathogenesis. Despite causing the majority of clinical cases, adaptive immunity resulting from classical Kp infections is poorly understood. Our laboratory has recently developed a model of adaptive immunity to live infection with classical Kp in which wild-type mice surviving primary infection are protected from morbidity and mortality upon rechallenge. Passive transfer of convalescent serum from surviving mice to naïve recipients does not confer protection against cKp infection, suggesting antibody responses alone are inadequate to protect against cKp. CD69+CD4+ T cells and γδ T cells expand dramatically in the lung following primary cKp infection and mice deficient in T cells are not protected from reinfection, indicating a requirement for T cells in the protective response. Further analysis of mice deficient in either classical αβ T cells or γδ T cells indicates that either T cell subset is capable of mediating protective immunity against Kp reinfection. Production of IL-17A by both CD4 and γδ T cells is enhanced during secondary infection. Together these data indicate that a natural course of infection with classical Kp elicits populations of classical T cells and γδ T cells that mediate protection against reinfection, likely through the rapid production of IL-17A. These results will ultimately inform rational design of vaccines and immunotherapies to prevent and treat Kp infection. Supported by AAI Careers in Immunology Fellowship