Offspring’s Tolerance of Mother Goes Viral Jeremy M. Kinder, Tony T. Jiang, Sing Sing Way  Immunity  Volume 44, Issue 5, Pages 1085-1087 (May 2016) DOI: 10.1016/j.immuni.2016.04.021 Copyright © 2016 Elsevier Inc. Terms and Conditions

Figure 1 Prenatal Exposure to Hepatitis B Virus-Infected Mothers Promotes Viral Persistence in Offspring In utero hepatitis B virus exposure from infected mothers dampens the anti-viral response in offspring, resulting in persistent viral infection. This is accomplished by skewing neonatal macrophages toward a tolerant phenotype (IL-10 production, arginase-1 [Arg1], and mannose receptor 1 [Mrc1] expression) and expression of PD-L1 to maintain a functionally exhausted phenotype for HBV-specific CD8+ T cells (left-sided panel). By contrast, when congenital hepatitis B virus exposure is eliminated in genetically identical offspring, a robust innate inflammatory response and T cell receptor (TCR) engagement by peptide + MHC (pMHCI) drives expansion of activated viral-specific CD8+ T cells resulting in self-resolving acute infection (right-sided panel). Immunity 2016 44, 1085-1087DOI: (10.1016/j.immuni.2016.04.021) Copyright © 2016 Elsevier Inc. Terms and Conditions