IL-17-Producing Innate and Pathogen-Specific Tissue Resident Memory {gamma}{delta} T Cells Expand in the Lungs of Bordetella pertussis-Infected Mice [INFECTIOUS DISEASE AND HOST RESPONSE]

T cells play a role in protective immunity to infection at mucosal surface, but also mediate pathology in certain autoimmune diseases through innate IL-17 production. Recent reports have suggested that T cells can have memory analogous to conventional αβ T cells. In this study we have examined the role of T cells in immunity to the respiratory pathogen Bordetella pertussis. T cells, predominantly V4^–1^– cells, produced IL-17 in the lungs as early as 2 h after infection. The bacterial burden during primary infection was significantly enhanced and the induction of antimicrobial peptides was reduced in the absence of early IL-17. A second peak of T cells is detected in the lungs 7–14 d after challenge and these T cells were pathogen specific. T cells, exclusively V4, from the lungs of infected but not naive mice produced IL-17 in response to heat-killed B. pertussis in the presence of APC. Furthermore, T cells from the lungs of mice reinfected with B. pertussis produced significantly more IL-17 than T cells from infected unprimed mice. T cells with a tissue resident memory T cell phenotype (CD69⁺CD103⁺) were expanded in the lungs during infection with B. pertussis and proliferated rapidly after rechallenge of convalescent mice. Our findings demonstrate that lung T cells provide an early source of innate IL-17, which promotes antimicrobial peptide production, whereas pathogen-specific V4 cells function in adaptive immunological memory against B. pertussis.

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