Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJDB11670 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| DRR294948.fastq.gz | Fastqsanger.gz | |||
| DRR294949.fastq.gz | Fastqsanger.gz | |||
| DRR294950.fastq.gz | Fastqsanger.gz | |||
| DRR294951.fastq.gz | Fastqsanger.gz | |||
| DRR294952.fastq.gz | Fastqsanger.gz |
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Project description:Expansion of B cell-helper T cells including T follicular helper (Tfh) and T peripheral helper (Tph) cells is a prominent feature of systemic lupus erythematosus (SLE), a prototypical autoimmune disease with broad autoantibody production. Human Tfh and Tph cells are marked by high production of the B cell chemoattractant CXCL13, yet regulation of T cell CXCL13 production and the relationship between a CXCL13+ state and other differentiated T cell states remains largely undefined. Here, we identify a dramatic imbalance in CD4 T cell phenotypes in SLE patients, with expansion of PD-1+/ICOS+ CXCL13+ T cells and reduction of CD96hi IL-22+ T cells. Using CRISPR screens, we identify the aryl hydrocarbon receptor (AHR) as a potent negative regulator of CXCL13 production by human CD4 T cells. Transcriptomic, epigenetic, and functional studies demonstrate that AHR coordinates with AP-1 family member JUN to prevent CXCL13+ Tph/Tfh cell differentiation and promote an IL-22+ phenotype. Type I interferon (IFN), a pathogenic driver of SLE, opposes AHR and JUN to promote T cell production of CXCL13. These results place CXCL13+ Tph/Tfh cells on a polarization axis opposite from Th22 cells and reveal AHR, JUN, and IFN as key regulators of these divergent T cell states.
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