GM‐CSF signalling in Th17‐cell pathogenicity: The culprit in autoimmune uveitis promoted by sleep loss

Abstract

Abstract Sleep loss (SL) is a health problem that affects autoimmune and inflammatory diseases. However, the relationship between SL, the immune system and autoimmune diseases remains unclear. This commentary summarizes and discusses the key findings of the study by Liu et al. published in Clinical and Translational Medicine. In this study, they analysed the effects of SL on autoimmune uveitis using mass cytometry, single‐cell RNA sequencing, and flow cytometry. They identified changes in the composition and function of human and mouse immune cells following SL that primarily involved effector CD4+ T cells and myeloid cells. Furthermore, they demonstrated that SL promoted Th17 differentiation, pathogenicity, and Interleukin‐23 (IL‐23)–Th17– granulocyte macrophage colony stimulating factor (GM‐CSF) feedback mechanism in autoimmunity. Finally, they attenuated SL‐induced EAU exacerbation using anti‐GM‐CSF treatment, providing a novel therapeutic approach for SL‐related autoimmune diseases.

Keywords

• autoimmune uveitis
• GM‐CSF
• mass cytometry
• single‐cell RNA sequencing
• sleep loss
• Th17 cells