| First Author | Liew PX | Year | 2017 |
| Journal | Immunity | Volume | 47 |
| Issue | 4 | Pages | 752-765.e5 |
| PubMed ID | 29045904 | Mgi Jnum | J:258615 |
| Mgi Id | MGI:6140479 | Doi | 10.1016/j.immuni.2017.09.016 |
| Citation | Liew PX, et al. (2017) iNKT Cells Orchestrate a Switch from Inflammation to Resolution of Sterile Liver Injury. Immunity 47(4):752-765.e5 |
| abstractText | After traumatic injury, some cells function as detectors to sense injury and to modulate the local immune response toward a restitution phase by affecting the local cytokine milieu. Using intravital microscopy, we observed that patrolling invariant natural killer T (iNKT) cells were initially excluded from a site of hepatic injury but subsequently were strategically arrested first via self-antigens and then by cytokines, circumscribing the injured site at exactly the location where monocytes co-localized and hepatocytes proliferated. Activation of iNKT cells by self-antigens resulted in the production of interleukin-4 (IL-4) but not interferon-gamma (IFN-gamma). This promoted increased hepatocyte proliferation, monocyte transition (from Ly6C(hi) to Ly6C(lo)), and improved healing where IL-4 from iNKT cells was critical for these processes. Disruption of any of these mechanisms led to delayed wound healing. We have shown that self-antigen-driven iNKT cells function as sensors and orchestrators of the transformation from inflammation to tissue restitution for essential timely wound repair. |
