Volume 153, Issue 5, Pages 1185-1187 (November 2017) Do Liver Mucosa-Associated Invariant T Cells Delay Hepatitis C Progression, or Are They Innocent Bystanders?  Mario U. Mondelli  Gastroenterology  Volume 153, Issue 5, Pages 1185-1187 (November 2017) DOI: 10.1053/j.gastro.2017.09.027 Copyright © 2017 AGA Institute Terms and Conditions

Figure 1 Mechanisms of intrahepatic mucosal-associated invariant T (MAIT) cell activation in hepatitis C virus (HCV) infection. Interleukin (IL)-7 and interferon (IFN)-α/β secreted by infected hepatocytes can directly activate MAIT cells, obviating to the limited IL-18 availability in the microenvironment resulting from dysfunctional monocytes. Impaired IFN-γ secretion occurs predominantly through T-cell receptor (TCR)-dependent MAIT cell activation by bacterial products. Treatment with direct-acting antivirals reduces expression of activation molecules by MAIT cells and their cytolytic potential, partially restoring MAIT cell homeostasis. Eomes, eomesodermin; L12R, IL12 receptor; IL18BPa, IL18 binding protein a; IL18R, IL18 receptor; LSEC, liver sinusoidal endothelial cell; Plzf, promyelocytic leukaemia zinc finger protein; RORγt, retinoic acid receptor (RAR)-related orphan receptor gamma t; T-bet, T box transcription factor; TNF, tumor necrosis factor. Gastroenterology 2017 153, 1185-1187DOI: (10.1053/j.gastro.2017.09.027) Copyright © 2017 AGA Institute Terms and Conditions