Research ArticleT CELLS

A distinct GM-CSF+ T helper cell subset requires T-bet to adopt a TH1 phenotype and promote neuroinflammation

See allHide authors and affiliations

Science Immunology  23 Oct 2020:
Vol. 5, Issue 52, eaba9953
DOI: 10.1126/sciimmunol.aba9953

You are currently viewing the editor's summary.

View Full Text

Log in to view the full text

Log in through your institution

Log in through your institution

Poised for pathogenicity

Production of GM-CSF by T helper cells not only guides adaptive immune responses but also can contribute to the pathogenesis of autoimmune disease. Rasouli et al. used single-cell RNA sequencing, mass cytometry, and GM-CSF fate mapper mice to identify a distinct subset of T helper cells in humans and mice that specialize in sustained GM-CSF production but lack key phenotypic features of other T helper lineages. In a murine model of experimental autoimmune encephalomyelitis, these cells were poised to up-regulate IFN-γ within the central nervous system and promote development of encephalitis, processes that required the transcription factor T-bet. These results provide insight into the identity of GM-CSF–producing CD4 T cells and their function during autoimmune neuroinflammation.

View Full Text

Stay Connected to Science Immunology