Communication between the central nervous system and the immune system involves a complex network of bidirectional communication. The functions of astrocytes, oligodendrocytes, neuronal stem cells, microglia and neurons do not happen in isolation, but are orchestrated by signals and interactions among each other. Signaling generated by inflammatory molecules produced by resident CNS cells or by intruding peripheral leukocytes alters the dynamics of cellular functions that often translate into detrimental actions for neurons. The mechanisms used by the neural tissue to avoid massive neuronal damage during autoimmune inflammation, infection and trauma has been extensively studied. However, the underlying mechanisms that link inflammation with action on/by glial cells and that ultimately lead to neuronal damage are vital to generate effective and long- lasting interventions for chronic CNS inflammation.
Subtopics include but are not limited to:
• Immune cells/molecules and interaction with nervous cells in health and animal models of disease or human disease
• Genomics, proteomic or bioinformatics studies
• Computational modeling
• Molecules that link immune and nervous system
• Regulation of cell-cell communication
• Regulation of neuronal damage and/or neurogenesis
• New methodologies to visualize or analyze interaction between glial cells and immune cells
• Participation of Innate and adaptive immunity in CNS plasticity
The aim of this Research Topic is to highlight interaction between inflammatory cells/molecules and the nervous system during acute and chronic inflammation. Studies from animal models, in vitro design, clinical, molecular, computational and biochemical perspectives that explore glial biology, inflammation and neuronal damage in original research or review papers are welcome.
Communication between the central nervous system and the immune system involves a complex network of bidirectional communication. The functions of astrocytes, oligodendrocytes, neuronal stem cells, microglia and neurons do not happen in isolation, but are orchestrated by signals and interactions among each other. Signaling generated by inflammatory molecules produced by resident CNS cells or by intruding peripheral leukocytes alters the dynamics of cellular functions that often translate into detrimental actions for neurons. The mechanisms used by the neural tissue to avoid massive neuronal damage during autoimmune inflammation, infection and trauma has been extensively studied. However, the underlying mechanisms that link inflammation with action on/by glial cells and that ultimately lead to neuronal damage are vital to generate effective and long- lasting interventions for chronic CNS inflammation.
Subtopics include but are not limited to:
• Immune cells/molecules and interaction with nervous cells in health and animal models of disease or human disease
• Genomics, proteomic or bioinformatics studies
• Computational modeling
• Molecules that link immune and nervous system
• Regulation of cell-cell communication
• Regulation of neuronal damage and/or neurogenesis
• New methodologies to visualize or analyze interaction between glial cells and immune cells
• Participation of Innate and adaptive immunity in CNS plasticity
The aim of this Research Topic is to highlight interaction between inflammatory cells/molecules and the nervous system during acute and chronic inflammation. Studies from animal models, in vitro design, clinical, molecular, computational and biochemical perspectives that explore glial biology, inflammation and neuronal damage in original research or review papers are welcome.