AhR promotes Th17 cells differentiation in chronic hepatitis B via JAK1/STAT3/SOCS3 pathway

Objectives：The mechanism of Th17/Treg imbalance in chronic hepatitis B (CHB)remains unclear. The aim of the study is to explore the immunopathogenesis of Th17/Treg imbalance in CHB through RNA transcriptome sequencing. Methods：This study included 15 instances in the healthy control (HC) and 15 cohortsin the chronic hepatitis B (CHB). Three patients from the CHB cohort and three participants from the HC subject were chosen at random. Their peripheral blood was used to separate CD4+ T cells, which were then subjected to RNA transcriptome sequencing. Finally, the RNA transcriptome sequencing results were validated by qRT-PCR and Western blotting. Results：differential genes AhR, HLA-DQA1/DQB1were directly involved in Th17 cell differentiation; while gene IL-7 took part in theJAK-STAT pathway, ATP6V1D, SLC7A5, SGK1 participated in the mTOR pathway, PIK3R3 and SOS1 were engaged in signaling pathways of mTOR and the JAK-STAT. C-X-C motif chemokine 10, TRAF4, and CEBPB were involved in the IL-17 signaling pathway. Conclusion：AhR may control Th17 cell development in CHB by activating the JAK1/STAT3/SOCS3 signaling pathway and regulated the Th17/Treg balance.