UNC93B1 Mediates Innate Inflammation and Antiviral Defense in the Liver during Acute Murine Cytomegalovirus Infection

Crane, Meredith J.; Gaddi, Pamela J.; Salazar-Mather, Thais P.

NK cell function in the absence of endosomal TLR signals contributes to inflated T cell responses. The presence of increased virus in the liver may also contribute to the robust T cell recruitment and cytokine production observed at late infection time points in 3d mice. Interestingly, although the severity of viral liver pathology was more pronounced in 3d mice, inflammation and liver injury subsided late in infection. These observations suggest that CD8+ T cells in the liver can respond to limited amounts of type I interferon for activation in the presence of compromised innate responses, emphasizing the prevalence of compensatory mechanisms in place within the liver to deal with infection and promote adaptive immunity. In contrast, IFN-a/bR deficiency negatively impacts innate inflammatory responses and resistance to MCMV infection in the liver [21, 24, 36] .