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CD8 α − conventional dendritic cells control V β T‐cell immunity in response to Staphylococcus aureus infection in mice
Author(s) -
Zhang Wei,
Xu Li,
Zhang Xiaoyan,
Xu Jianqing,
Jin JunO
Publication year - 2020
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1111/imm.13171
Subject(s) - staphylococcus aureus , immune system , spleen , biology , cd8 , acquired immune system , dendritic cell , immunity , immunology , t cell , cytotoxic t cell , microbiology and biotechnology , in vitro , bacteria , biochemistry , genetics
Dendritic cells (DCs) are potent immune cells that control innate and adaptive immune responses. Previous studies have shown that the DCs are required for protection against Staphylococcus aureus infection. However, the role of conventional DC (cDC) subsets during S. aureus infection in vivo has not been well investigated. In this study, we examined the function of spleen DC subsets in the activation of immunity against S. aureus infection. C57BL/6 mice were infected intravenously with S. aureus and DC and T‐cell activation were analyzed in vivo . We found that the spleen CD8 α − cDCs phagocytosed S. aureus more efficiently than type‐1 conventional DCs (cDC1s) did. Moreover, the CD8 α − cDCs contributed to the production of pro‐inflammatory cytokines in response to S. aureus infection , whereas the cDC1s did not. In addition, infection with S. aureus promoted an increase in the number of V β T cells. The CD4 + and CD8 + V β T cells up‐regulated the production of interferon‐ γ (IFN‐ γ ) and interleukin‐17 (IL‐17) in response to S. aureus infection. Importantly, the induction of IFN‐ γ and IL‐17 production in CD4 + and CD8 + V β T cells was mediated by S. aureus ‐stimulated CD8 α − cDCs, whereas cDC1s failed to promote IFN‐ γ and IL‐17 production in the cells. Therefore, these data suggested that the spleen CD8 α − cDCs are the main DC subsets for induction of S. aureus superantigen‐specific immunity.