Editor’s summary Modulating plasticity in pathogenic T cells to promote a tolerogenic phenotype is a promising therapeutic approach in autoimmunity and cancer. To explore how pathogenic TH17 cell plasticity is regulated in mouse models of kidney and gut inflammation, Enk et al. optimized an in vivo pooled single-cell CRISPR droplet sequencing (iCROP-seq) screen. iCROP-seq enabled the assessment and quantification of CRISPR-modified TH17 cell polarization states in vivo.
