Astrocytes strongly contribute to CNS immune responses. Through endfeet, they contribute
Astrocytes strongly contribute to CNS immune responses. Through endfeet, they contribute to the formation and maintenance of the blood-brain barrier (BBB) and perivascular space, thereby controlling immune cell entry. Astrocytes respond to injury or infection Astrocytes strongly contribute to CNS immune responses. Through endfeet, they contribute to the formation and maintenance of the blood-brain barrier (BBB) and perivascular space, thereby controlling immune cell entry. Astrocytes respond to injury or infection through a process termed reactive astrogliosis (3), characterized by morphological and transcriptional changes that can either limit damage or contribute to chronic inflammation. In both physiological and pathological contexts, astrocytes secrete cytokines, chemokines, and growth factors controlling reactive microgliosis and peripheral immune cell recruitment. Astrocytes also regulate extracellular ion balance, neurotransmitter clearance, and metabolic support, all of which indirectly shape inflammatory signaling (4). Oligodendrocytes and OPCs, while primarily involved in myelination, also participate in immune interactions and synaptic pruning and are particularly vulnerable to immune-mediated damage. Finally, ependymal glia control CNS-cerebrospinal fluid (CSF) communications involved in the regulation of CNS immunity. Together, these glial populations form an integrated immunological framework essential for maintaining homeostasis of the nervous tissue and coordinating protective responses. a process termed reactive astrogliosis (3), characterized by morphological and transcriptional changes that can either limit damage or contribute to chronic inflammation. In both physiological and pathological contexts, astrocytes secrete cytokines, chemokines, and growth factors controlling reactive microgliosis and peripheral immune cell recruitment. Astrocytes also regulate extracellular ion balance, neurotransmitter clearance, and metabolic support, all of which indirectly shape inflammatory signaling (4). Oligodendrocytes and OPCs, while primarily involved in myelination, also participate in immune interactions and synaptic pruning and are particularly vulnerable to immune-mediated damage. Finally, ependymal glia control CNS-cerebrospinal fluid (CSF) communications involved in the regulation of CNS immunity. Together, these glial populations form an integrated immunological framework essential for maintaining homeostasis of the nervous tissue and coordinating protective responses. When dysregulated, they contribute to the pathogenesis of neuroinflammatory and neurodegenerative disorders.This research topic aims to explore the potential immune functions of different glial cell types and their interactions with peripheral immune cells that modulate immune responses, and to address the underlying mechanisms, which are often related but not limited to macrogliamicroglia interactions.The review by Haroon et al. provides an overview of what is known about the recently recognized immune capabilities of OPCs, including phagocytosis of myelin debris and the engulfment of axons and presynaptic terminals via low-density lipoprotein receptor-related protein 1 (LRP1). In addition, the authors discuss OPCs' ability to release specific cytokines that regulate the activation and recruitment of immune cells. A subset of OPCs can even present antigen to T cells by expressing major histocompatibility complexes, contributing to the pathogenesis of Multiple Sclerosis (MS). Thus, the functions of OPCs are far more complex than we have anticipated thus far. Similar to what has been described for microglia, oligodendrocytes and OPCs may also possess disease-associated subtypes that differ from those that contribute to myelin formation under homeostatic conditions (5).The MS usually starts with a relapsing-remitting form that then later converts to a progressive form with age and duration of the disease. Atkinson et al. summarize the contribution of microglia to CNS infiltration by T cells, driving the progressive phase of MS and its animal models during aging. The latter specifically target oligodendroglial cells and impair their potential to myelinate. The authors present evidence for the beneficial effects of senolytic therapies on clinical scores in a mouse model of MS, using middle-aged rather than young mice, highlighting the importance of individual patients' age for their vulnerability to disease progression and their responsiveness to therapies. Thus, the interplay between microglia and T cells can modulate the microenvironment of OPCs and thereby influence their remyelination efficiency.Trypanosoma brucei. They show that the parasite load increases in the CSF but not in the brain parenchyma, despite obvious early reactive microgliosis. These findings highlight the important role of microglia in brain protection and their capacity to fight parasitic infection together with infiltrating peripheral …
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