The healthy central nervous system (CNS) harbours an ontogenetically heterogeneous pool of myeloid cells that facilitates the maintenance of tissue integrity and function during development, adulthood and senescence. Only recently the advent of novel single-cell-based technologies such as high-dimensional mass spectrometry or RNA sequencing (scRNA-seq) in combination with unbiased computational tools, has allowed for the identification of various CNS myeloid subsets with distinct functions during homeostasis and disease. It is now evident that the CNS accommodates a complex phenotypical and functional heterogeneity within this innate immune cell compartment even under steady-state conditions, that is only surpassed by the reactive cellular diversity during pathology. At large, CNS-resident myeloid cells can be discerned into parenchymal cells (such as microglia) and the non-parenchymal compartment including dendritic cells and macrophages, all of which occupy uniquely assigned tasks within the continuous maintenance of tissue homeostasis and immune surveillance
Ample studies have revealed involvement of discrete myeloid subsets in both the emergence and resolution of acquired CNS pathologies including inflammatory, degenerative, and vascular conditions. Especially during disease, CNS resident myeloid cells are complemented by the migration and recruitment of blood-borne monocyte-derived cells, adding further to the cellular complexity in the CNS and its interfaces. Myeloid cells in the CNS mediate synapse development, plasticity, scavenge material, patrol against invading pathogens, facilitate tissue repair, and function as antigen presenting cells. While in recent years a tremendous body of research has shed light on the diversity of CNS resident/infiltrating myeloid cells and helped in the phenotypical characterisation of these subsets, only little is known on how to harness this knowledge to mitigate disease. Hence, a granular understanding of CNS myeloid cell function during homeostasis and pathology is warranted in order to develop novel myeloid cell-targeting therapeutic strategies in the treatment of CNS diseases.
This research topic welcomes contributions (including e.g. original research, reviews, perspectives, commentaries, opinions, hypothesis & theory articles). We hope for this Research Topic to provide a deeper understanding of the cellular and molecular underpinnings of CNS disorders, the role of myeloid cells therein and to identify new and innovative therapeutic avenues. We welcome submissions based on (but not limited to) the following topics:
• Human and animal studies on the function of myeloid cell subsets with CNS resident cells
• Function of myeloid cell subsets within CNS pathology
• Translational applications of myeloid cells in the mitigation of disease
• Novel myeloid cell-targeting therapeutic strategies
Benjamin Segal has recently worked as a consultant for Neurodiem, a lecturer for the Advanced Curriculum for Multiple Sclerosis CME course, and worked as a consultant for Banner Life Sciences, Senda Biosciences, and Ely Lily. All of the other topic editors have no conflicts of interest
The healthy central nervous system (CNS) harbours an ontogenetically heterogeneous pool of myeloid cells that facilitates the maintenance of tissue integrity and function during development, adulthood and senescence. Only recently the advent of novel single-cell-based technologies such as high-dimensional mass spectrometry or RNA sequencing (scRNA-seq) in combination with unbiased computational tools, has allowed for the identification of various CNS myeloid subsets with distinct functions during homeostasis and disease. It is now evident that the CNS accommodates a complex phenotypical and functional heterogeneity within this innate immune cell compartment even under steady-state conditions, that is only surpassed by the reactive cellular diversity during pathology. At large, CNS-resident myeloid cells can be discerned into parenchymal cells (such as microglia) and the non-parenchymal compartment including dendritic cells and macrophages, all of which occupy uniquely assigned tasks within the continuous maintenance of tissue homeostasis and immune surveillance
Ample studies have revealed involvement of discrete myeloid subsets in both the emergence and resolution of acquired CNS pathologies including inflammatory, degenerative, and vascular conditions. Especially during disease, CNS resident myeloid cells are complemented by the migration and recruitment of blood-borne monocyte-derived cells, adding further to the cellular complexity in the CNS and its interfaces. Myeloid cells in the CNS mediate synapse development, plasticity, scavenge material, patrol against invading pathogens, facilitate tissue repair, and function as antigen presenting cells. While in recent years a tremendous body of research has shed light on the diversity of CNS resident/infiltrating myeloid cells and helped in the phenotypical characterisation of these subsets, only little is known on how to harness this knowledge to mitigate disease. Hence, a granular understanding of CNS myeloid cell function during homeostasis and pathology is warranted in order to develop novel myeloid cell-targeting therapeutic strategies in the treatment of CNS diseases.
This research topic welcomes contributions (including e.g. original research, reviews, perspectives, commentaries, opinions, hypothesis & theory articles). We hope for this Research Topic to provide a deeper understanding of the cellular and molecular underpinnings of CNS disorders, the role of myeloid cells therein and to identify new and innovative therapeutic avenues. We welcome submissions based on (but not limited to) the following topics:
• Human and animal studies on the function of myeloid cell subsets with CNS resident cells
• Function of myeloid cell subsets within CNS pathology
• Translational applications of myeloid cells in the mitigation of disease
• Novel myeloid cell-targeting therapeutic strategies
Benjamin Segal has recently worked as a consultant for Neurodiem, a lecturer for the Advanced Curriculum for Multiple Sclerosis CME course, and worked as a consultant for Banner Life Sciences, Senda Biosciences, and Ely Lily. All of the other topic editors have no conflicts of interest
