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IL-17-Producing Innate and Pathogen-Specific Tissue Resident Memory gamma delta T Cells Expand in the Lungs of Bordetella pertussis-Infected Mice
Ist Teil von
The Journal of immunology (1950), 2017-01, Vol.198 (1), p.363-374
Erscheinungsjahr
2017
Quelle
EZB Electronic Journals Library
Beschreibungen/Notizen
gamma delta 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 gamma delta T cells can have memory analogous to conventional alpha beta T cells. In this study we have examined the role of gamma delta T cells in immunity to the respiratory pathogen Bordetella pertussis. gamma delta T cells, predominantly V gamma 4- gamma 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 gamma delta T cells is detected in the lungs 7-14 d after challenge and these gamma delta T cells were pathogen specific. gamma delta T cells, exclusively V gamma 4, 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, gamma delta T cells from the lungs of mice reinfected with B. pertussis produced significantly more IL-17 than gamma delta T cells from infected unprimed mice. gamma delta 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 gamma delta T cells provide an early source of innate IL-17, which promotes antimicrobial peptide production, whereas pathogen-specific V gamma 4 cells function in adaptive immunological memory against B. pertussis.