Editorial: Glial cells and immune cells in neuroinflammatory and neurodegenerative diseases

Immune dysfunction and inflammation are involved in autoimmune neurological and neurodegenerative disorders (NDs) (Tansey et al., 2022). It is now clear that the dysfunction of glial cells, including microglia, astrocytes and oligodendrocytes, contributes to neuroinflammation in disease pathogenesis. Genome-wide association studies have identified some disease-associated gene mutations that are highly expressed in glial cells, which lead to autonomous disturbances of glial cells and may initiate diseases or induce neuroinflammation to contribute to disease pathogenesis (Shi and Holtzman, 2018). Recently, emerging novel genomic technologies have enabled the characterization of distinct types of glial cells in response to distinct disease conditions (Colonna and Brioschi, 2020). The temporal and spatial heterogeneity of glial cells has either beneficial or detrimental effects on disease progression. Moreover, bidirectional communication between glial cells in the central nervous system (CNS) and other immune cells in the peripheral tissues is essential for brain homeostasis. Disorders of the peripheral immune cells also contribute to the reactivity of glial cells in the CNS (Tansey et al., 2022). The manuscripts in this Research Topic focus on the mechanism underlying how glial cells contribute to the pathogenesis of neurodegeneration and other neuroinflammatory disorders. We highlight two specific themes in this topic: (1) the roles of neuroinflammation caused by glial cell dysfunction in disease pathogenesis and (2) the heterogeneity of glial cells in response to disease-associated conditions.