PD-1 deficiency reshapes the TCRB repertoire and T-cell developmental programs associated with susceptibility to lupus-like autoimmunity
Programmed cell death protein-1 (PD-1) is a critical immune checkpoint. We utilized immune repertoire sequencing (IR-seq) and bulk RNA-sequencing (RNA-seq) to investigate the impact of PD-1 deficiency on the T-cell receptor (TCR) repertoire and transcriptomic landscape in mice. Peripheral blood mononuclear cells (PBMCs) were collected from wild-type, PD-1 heterozygous, and PD-1-deficient C57BL/6N mice. Our findings demonstrate that PD-1 deficiency is associated with altered TCRB repertoire organization, including shifted CDR3 length distributions and skewed TRBV/TRBJ segment usage, alongside transcriptional changes in genes linked to lymphocyte development and repertoire maintenance. Furthermore, we evaluated disease susceptibility by establishing an infection-triggered lupus-like autoimmune model using formaldehyde-inactivated Campylobacter jejuni (CJ-S131). The multi-omics data reveal that impaired PD-1 signaling creates a baseline immunological landscape that increases susceptibility to environmentally triggered lupus-like autoimmunity. This BioProject encompasses the raw IR-seq and RNA-seq reads supporting these findings.