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iNKT Cells Orchestrate a Switch from Inflammation to Resolution of Sterile Liver Injury.

Immunity | Oct 17, 2017

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-γ (IFN-γ). This promoted increased hepatocyte proliferation, monocyte transition (from Ly6Chi to Ly6Clo), 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.

Pubmed ID: 29045904 RIS Download

Mesh terms: Animals | Autoantigens | Cell Proliferation | Hepatocytes | Inflammation | Interleukin-4 | Kupffer Cells | Liver | Mice, Inbred BALB C | Mice, Inbred C57BL | Mice, Knockout | Mice, Transgenic | Microscopy, Confocal | Microscopy, Fluorescence, Multiphoton | Monocytes | Natural Killer T-Cells | Time Factors | Wound Healing

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Associated grants

  • Agency: CIHR, Id: FDN-143248

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