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. Author manuscript; available in PMC: 2016 Apr 1.
Published in final edited form as: Hepatology. 2015 Feb 4;61(4):1163–1173. doi: 10.1002/hep.27634

Fig. 6. Schematic model for premature T cell aging by HCV-induced, miR-181a-mediated DUSP6 regulatory signaling pathways.

Fig. 6

HCV-induced decline of miR-181a expression facilitates DUSP6 over-expression in CD4+ T cells. This, in turn, may negatively affect the TCR-induced signaling pathways, such as ERK/MAPK phosphorylation and then alters cell cycle regulators p21cip1/p27kip1 and cyclins and cyclin-dependent kinases (CDKs) activities. Therefore, reconstitution of miR-181a and/or inhibition of DUSP6 may provide a novel approach to improve T cell responses in virally infected individuals.