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Antibody opsonization enhances MAIT cell responsiveness to bacteria via a TNF ‐dependent mechanism
Author(s) -
Bánki Zoltán,
Krabbendam Lisette,
Klaver Dominik,
Leng Tianqi,
Kruis Simon,
Mehta Hema,
Müllauer Brigitte,
OrthHöller Dorothea,
Stoiber Heribert,
Willberg Christian B,
Klenerman Paul
Publication year - 2019
Publication title -
immunology and cell biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.999
H-Index - 104
eISSN - 1440-1711
pISSN - 0818-9641
DOI - 10.1111/imcb.12239
Subject(s) - antibody opsonization , tumor necrosis factor alpha , cytokine , microbiology and biotechnology , biology , antibody , chemistry , immunology , opsonin
Mucosal‐associated invariant T ( MAIT ) cells are an abundant human T‐cell subset with antimicrobial properties. They can respond to bacteria presented via antigen‐presenting cells ( APC s) such as macrophages, which present bacterially derived ligands from the riboflavin synthesis pathway on MR 1. Moreover, MAIT cells are also highly responsive to cytokines which enhance and even substitute for T‐cell receptor‐mediated signaling. The mechanisms leading to an efficient presentation of bacteria to MAIT cells by APC s have not been fully elucidated. Here, we showed that the monocytic cell line THP ‐1 and B cells activated MAIT cells differentially in response to Escherichia coli . THP ‐1 cells were generally more potent in inducing IFN γ and IFN γ/ TNF production by MAIT cells. Furthermore, THP ‐1, but not B, cells produced TNF upon bacterial stimulation, which in turn supported IFN γ production by MAIT cells. Finally, we addressed the role of antibody‐dependent opsonization of bacteria in the activation of MAIT cells using in vitro models. We found that opsonization had a substantial impact on downstream MAIT cell activation by monocytes. This was associated with enhanced activation of monocytes and increased TNF release. Importantly, this TNF acted in concert with other cytokines to drive MAIT cell activation. These data indicate both a significant interaction between adaptive and innate immunity in the response to bacteria, and an important role for TNF in MAIT cell triggering.