Journal
MUCOSAL IMMUNOLOGY
Volume 13, Issue 3, Pages 460-470Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/s41385-019-0246-1
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Funding
- Joint Liverpool University-China Scholarship Council (CSC) Scholarship
- SPARKS Medical Research, Cancer Research Wales PhD studentship
- Medical Research Council UK
- MRC [MR/P011284/1] Funding Source: UKRI
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The human nasopharynx is frequently exposed to microbial pathogens, including superantigen-producing Staphylococcus aureus (SAg-Sau), which activates potent pro-inflammatory T cell responses. However, cellular mechanisms that control SAg-Sau-driven T cell activation are poorly understood. Using human nasopharynx-associated lymphoid tissue (NALT), we show that SAg-Sau drove a strong Th17 activation, which was associated with an impaired CD4(+) T cell-mediated immune regulation. This impairment of immune control correlated with a significant downregulation of interleukin-35 (IL-35) expression in tonsillar CD4(+) T cells by SAg-Sau. Supplementing recombinant IL-35 suppressed SAg-Sau-activated Th17 responses, and this IL-35-mediated suppression positively correlated with the level of Th17 activation. Interestingly, SAg-Sau stimulation induced Foxp3(+) Treg expansion and interleukin-10 (IL-10) production, which effectively suppressed the Th1 response, but failed to control the activation of Th17 cells. Overall, our results reveal an aberrant T cell regulation on SAg-Sau-driven Th17 activation and identify IL-35 as a critical cytokine to control superantigenic S.aureus-activated Th17 responses.
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