| First Author | Greco SH | Year | 2016 |
| Journal | J Leukoc Biol | Volume | 100 |
| Issue | 1 | Pages | 185-94 |
| PubMed ID | 26747838 | Mgi Jnum | J:243089 |
| Mgi Id | MGI:5907581 | Doi | 10.1189/jlb.3A0515-185R |
| Citation | Greco SH, et al. (2016) Mincle suppresses Toll-like receptor 4 activation. J Leukoc Biol 100(1):185-94 |
| abstractText | Regulation of Toll-like receptor responses is critical for limiting tissue injury and autoimmunity in both sepsis and sterile inflammation. We found that Mincle, a C-type lectin receptor, regulates proinflammatory Toll-like receptor 4 signaling. Specifically, Mincle ligation diminishes Toll-like receptor 4-mediated inflammation, whereas Mincle deletion or knockdown results in marked hyperresponsiveness to lipopolysaccharide in vitro, as well as overwhelming lipopolysaccharide-mediated inflammation in vivo. Mechanistically, Mincle deletion does not up-regulate Toll-like receptor 4 expression or reduce interleukin 10 production after Toll-like receptor 4 ligation; however, Mincle deletion decreases production of the p38 mitogen-activated protein kinase-dependent inhibitory intermediate suppressor of cytokine signaling 1, A20, and ABIN3 and increases expression of the Toll-like receptor 4 coreceptor CD14. Blockade of CD14 mitigates the increased sensitivity of Mincle(-/-) leukocytes to Toll-like receptor 4 ligation. Collectively, we describe a major role for Mincle in suppressing Toll-like receptor 4 responses and implicate its importance in nonmycobacterial models of inflammation. |
