Murine gamma delta intraepithelial lymphocyte response to type I IFN and TCR blockade
Interferon alpha (IFNa) is a pro-inflammatory cytokine that is rapidly upregulated as part of an innate immune response. Gamma delta intraepithelial lymphocytes (gd IEL) mount a rapid antimicrobial response to luminal microorganisms and previous report indicate that the T cell receptor (TCR) of these cells is constantly triggered at steady-state. We assessed the contribution of tonic TCR activation in response to acute, systemic IFNa administration among murine gd IELs. Our data demonstrate that inhibiting basal TCR signaling has a minimal effect on the transcriptional profile of gd IELs and acute IFNa exposure induces antiviral gene programs independent of TCR signaling. Overall design: Mice were treated mice with 200 ug TCRgd antibody (UC7-13D5) or Armenian hamster IgG i.p. (-48 or -24 h) prior to i.v. administration with 1 ug murine IFNa or phosphate buffered saline (PBS) for 5 h. RNAseq was performed on sorted gd IELs isolated from murine small intestine from each of the following treatment groups: IgG-PBS, IgG-IFNa, UC713D5-PBS, UC713D5-IFNa