IL-17A/F enable cholangiocytes to restrict T cell-driven experimental cholangitis by upregulating PD-L1 expression.

ABSTRACT:

Background & aims

IL-17A-producing T cells are present in autoimmune cholestatic liver diseases; however, little is known about the contribution of IL-17 to periductal immune responses. Herein, we investigated the role of IL-17 produced by antigen-specific CD8⁺ T cells in a mouse model of cholangitis and in vitro in human cholangiocyte organoids.

Methods

K14-OVAp mice express a major histocompatibility complex I-restricted ovalbumin (OVA) peptide sequence (SIINFEKL) on cholangiocytes. Cholangitis was induced by the adoptive transfer of transgenic OVA-specific ovalbumin transgene (OT)-1 CD8⁺ T cells that either had OT-1^wt or lacked IL-17A/F (OT-1^IL17ko). The response of mouse and human cholangiocytes/organoids to IL-17A was assessed

SUBMITTER: Stein S 

PROVIDER: S-EPMC8778963 | biostudies-literature | 2021 Apr

REPOSITORIES: biostudies-literature