Abstract
Mucosal-associated invariant T (MAIT) cells are an innate-like population of T cells that display a TCR Vα7.2+ CD161+ phenotype and are restricted by the nonclassical MHC-related molecule 1 (MR1). Although B cells control MAIT cell development and function, little is known about the mechanisms underlying their interaction(s). Here, we report, for the first time, that during Salmonella enterica serovar Typhi (S. Typhi) infection, HLA-G expression on B cells downregulates IFN-γ production by MAIT cells. In contrast, blocking HLA-G expression on S. Typhi-infected B cells increases IFN-γ production by MAIT cells. After interacting with MAIT cells, kinetic studies show that B cells upregulate HLA-G expression and downregulate the inhibitory HLA-G receptor CD85j on MAIT cells resulting in their loss. These results provide a new role for HLA-G as a negative feedback loop by which B cells control MAIT cell responses to antigens.
Highlights
Mucosal-associated invariant T (MAIT) cells are innate-like T-cells restricted by the nonclassical MHC-related molecule 1 (MR1) that exhibit a T cell receptor (TCR) Va7.2+ CD161+ phenotype [1,2,3,4]
We observed that CD161 mean fluorescence intensity (MFI), a measurement of the mean expression levels per cell, was significantly decreased in MAIT cells exposed to INF B-lymphoblastoid cell lines (B-LCLs) (Figure S1D)
These results suggested that changes in CD161 expression on MAIT cells was dependent on B cell interaction and decreases in their expression levels due to S
Summary
MAIT cells are innate-like T-cells restricted by the nonclassical MHC-related molecule 1 (MR1) that exhibit a TCR Va7.2+ CD161+ phenotype [1,2,3,4]. MAIT cells have broad anti-microbial reactivity and can mediate strong immune responses to bacteria such as Mycobacterium tuberculosis (Mtb), Vibrio cholera, Escherichia coli (E. coli), Shigella, Helicobacter pylori, S. B cells are major antigen-presenting cells during the initial [12] and re-stimulation phases [13] of host immune responses. Activated B cells express the Lectin-like transcript-1 (LLT1) molecule, the CD161 ligand on the MAIT cell membrane surface [24,25,26,27].
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