Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS). Oxidative stress and the production of reactive oxygen species (ROS) are hallmarks of the tissue-damaging inflammatory process in MS. Determining the identity of tissue-damaging cells in the CNS and characterizing the molecular mechanisms that propagate oxidative stress-mediated pathology is a focus of MS research.

In this preprint (not peer reviewed), Villar-Vesga et al. analysed human and mouse transcriptomic datasets to establish gene signatures of oxidative stress across immune cell populations in the healthy and diseased MS brain. Focusing their investigation on macrophages, the largest immune cell population in the CNS, they identified that tissue-invading monocyte-derived cells, rather than resident microglia, express the highest levels of ROS-associated genes in neuroinflammation. Using mice with experimental autoimmune encephalomyelitis (EAE), a pre-clinical model of MS, they validated ROS production by flow cytometry, confirming the observations of their in silico analysis.