T cell-selective deletion of Oct1 protects animals from autoimmune neuroinflammation while maintaining neurotropic pathogen response.

ABSTRACT:

Background

Treatments for autoimmune diseases aim to dampen autoreactivity while preserving normal immune function. In CD4⁺ T cells, the transcription factor Oct1/Pou2f1 is a dispensable transcription factor for T cell development and response to primary infection, but promotes expression of target genes, including Il2 and Ifng, under conditions of antigen reencounter. As a result, they are more strongly expressed upon secondary stimulation. Such repeated antigen encounters occur in memory recall responses, in autoimmunity where self-antigen can be recognized multiple times, and in chronic infection where foreign antigen is persistent. Based on these previous findings, we hypothesized that Oct1 loss would protect animals from autoimmunity but maintain normal responses to

SUBMITTER: Kim H 

PROVIDER: S-EPMC6607600 | biostudies-literature | 2019 Jul

REPOSITORIES: biostudies-literature