2020
DOI: 10.1016/j.celrep.2020.01.040
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TLR9 Sensing of Self-DNA Controls Cell-Mediated Immunity to Listeria Infection via Rapid Conversion of Conventional CD4+ T Cells to Treg

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Cited by 11 publications
(10 citation statements)
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“…Monocyte-derived DCs stimulated with TLR4 and TLR7/8 ligands induce naive allogeneic CD4 + T cells to secrete IL-10 and IFN-γ sequentially and eventually IL-17A ( 107 ). The activation of TLR9 and IL-12 pathways in CD8α + DCs can drive CD4 + T cells to act as Th cells or induce rapid polyclonal conversion to immunosuppressive Treg during Listeria infection ( 108 ). Interestingly, although all TLRs on DCs are able to induce CD8 + T cell activation in vitro , the abilities of surface and endosomal TLRs to activate CD8 + T cells might be different in vivo .…”
Section: Tlr-mediated Regulation Of Apcsmentioning
confidence: 99%
“…Monocyte-derived DCs stimulated with TLR4 and TLR7/8 ligands induce naive allogeneic CD4 + T cells to secrete IL-10 and IFN-γ sequentially and eventually IL-17A ( 107 ). The activation of TLR9 and IL-12 pathways in CD8α + DCs can drive CD4 + T cells to act as Th cells or induce rapid polyclonal conversion to immunosuppressive Treg during Listeria infection ( 108 ). Interestingly, although all TLRs on DCs are able to induce CD8 + T cell activation in vitro , the abilities of surface and endosomal TLRs to activate CD8 + T cells might be different in vivo .…”
Section: Tlr-mediated Regulation Of Apcsmentioning
confidence: 99%
“… 26 There is accumulative evidence suggesting the interactions between DNA and CD4 + T cells. Recent studies have shown the conversion of conventional CD4 + T cells into Tregs due to exposure of self‐DNA in Listeria infection 61 and self‐DNA induced stimulation of activated CD4 + T cells. 62 These studies point towards some of the implications of this unexplored interaction of adaptive immune cells and innate immune triggers in health and disease.…”
Section: Discussionmentioning
confidence: 99%
“…In practice, however, some PRRs have not been proven to bind directly to cryptococcal cells, which makes it important to carefully consider whether they are true PRRs. Because PRRs also recognize the so-called alarmins, including self-DNA, HMGB1, and S100A9, they can also respond to the alarmins that emerge after response to a cryptococcal stimuli [39][40][41][42]. Even in this case, because cytokine production can be reduced after cryptococcal stimulation in PRRs-deficient cells, it may not be possible to accurately determine whether the PRRs recognize cryptococcus-induced alarmins or cryptococcal cells itself.…”
Section: Discussionmentioning
confidence: 99%