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CCR2 Inflammatory Dendritic Cells and Translocation of Antigen by Type III Secretion Are Required for the Exceptionally Large CD8 T Cell Response to the Protective YopE Epitope during Infection
Dendritic cells (DCs) direct host protective adaptive immune responses during infection. How different subpopulations of DCs contribute to the formation of antigen-specific CD8+ T cells is incompletely understood. Infection of C57BL/6 mice with the bacterial pathogen Yersinia pseudotuberculosis results in the production of an exceptionally large CD8+ T cell response to an epitope in the type III secretion system effector YopE. Here, we show that this large CD8+ T cell response requires translocation of YopE into inflammatory DCs, which express CCR2 and accumulate in infected tissues. In contrast, when mice are infected with a Y. pseudotuberculosis strain that can secrete but not translocate YopE, a smaller response is seen, and under these conditions the generation of YopE-specific CD8+ T cell requires CD8α+ DCs. Our results indicate that distinct DC subsets participate in constructing the CD8+ T cell response to secreted, versus translocated, YopE. Furthermore our data indicate that inflammatory DCs are a driving force behind the massive CD8+ T cell response to a protective epitope in a bacterial virulence factor that is translocated into host cells.
Vyšlo v časopise: CCR2 Inflammatory Dendritic Cells and Translocation of Antigen by Type III Secretion Are Required for the Exceptionally Large CD8 T Cell Response to the Protective YopE Epitope during Infection. PLoS Pathog 11(10): e32767. doi:10.1371/journal.ppat.1005167
Kategorie: Research Article
prolekare.web.journal.doi_sk: https://doi.org/10.1371/journal.ppat.1005167Souhrn
Dendritic cells (DCs) direct host protective adaptive immune responses during infection. How different subpopulations of DCs contribute to the formation of antigen-specific CD8+ T cells is incompletely understood. Infection of C57BL/6 mice with the bacterial pathogen Yersinia pseudotuberculosis results in the production of an exceptionally large CD8+ T cell response to an epitope in the type III secretion system effector YopE. Here, we show that this large CD8+ T cell response requires translocation of YopE into inflammatory DCs, which express CCR2 and accumulate in infected tissues. In contrast, when mice are infected with a Y. pseudotuberculosis strain that can secrete but not translocate YopE, a smaller response is seen, and under these conditions the generation of YopE-specific CD8+ T cell requires CD8α+ DCs. Our results indicate that distinct DC subsets participate in constructing the CD8+ T cell response to secreted, versus translocated, YopE. Furthermore our data indicate that inflammatory DCs are a driving force behind the massive CD8+ T cell response to a protective epitope in a bacterial virulence factor that is translocated into host cells.
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Hygiena a epidemiológia Infekčné lekárstvo Laboratórium
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