C-C chemokine receptor type 7 (CCR7) regulates hepatic CD8+ T cell homeostasis and response to acute liver injury - Nanostring gene expression data

Acute liver failure (ALF) is a rare but life-threatening condition, and drug-induced liver injury (DILI), particularly acetaminophen (APAP) toxicity, is the leading cause of ALF. Innate immune mechanisms further perpetuate liver injury, while the role of the adaptive immune system in DILI-related ALF is unclear. 
We analyzed liver tissue from two independent patient cohorts with ALF and identified hepatic T cell infiltration as a prominent feature in human ALF. CD8+ T cells were characterised by zonation towards necrotic regions and an activated gene expression signature. In murine APAP-induced liver injury, intravital microscopy revealed zonation of CD8+ but not CD4+ T cells at necrotic areas. Gene expression analysis exposed pregulated C-C chemokine receptor 7 (CCR7) and its ligand CCL21 in liver as well as a broadly activated phenotype of hepatic CD8+ T cells. In two mouse models of ALF, Ccr7-/- mice had significantly aggravated early-phase liver damage. Functionally, CCR7 was not involved in the recruitment of CD8+ T cells, but regulated their activation profile potentially via egress to lymphatics. Ccr7-/- CD8+ T cells were characterized by elevated expression of activation, effector, and exhaustion profiles.

In this data set, gene expression of sorted CD4+ or CD8+ T-cells from  liver leukocyte extracts of either WT or CCR7-knock-out mice that were either untreated or challenged with APAP was measured using the nCounter Mouse Immunology Kit.