About this Research Topic
Innate immune signaling in the central nervous system (CNS) extends beyond the direct role of resident cells such as microglia and mast cells, and more broadly encompasses signaling via innate cytokines, pattern recognition receptors (PRRs), inflammasomes, complement and others. In the periphery, these signaling events are commonly associated with inflammation, infection and the progression of disease.
However, it is increasingly evident that similar innate immune signaling activities can have either a physiological or pathological role during development, homeostasis and acute injury in the CNS. For instance, signaling by complement and TGFβ guides both the synaptic pruning by microglia during development and the downregulation of this process in the healthy adult brain. Similarly, the IL-1 family cytokine, IL-33, which is secreted by neurons directs microglia to promote neuronal spine plasticity to aid memory consolidation. However, excessive pruning in response to IL-33 causes neuronal damage associated with schizophrenia.
There is a growing interest in the role of inflammatory cytokines (i.e. IL-1β) and inflammasomes in brain development and injury including hypoxia and ischemia. Intriguingly, cell-type-specific IL-1 receptor1 (IL-1R1) signaling in the CNS guides distinct neuronal functions and behavioral responses. Targeting this part of innate immunity has heralded great therapeutic promise in the neurodegenerative space. In the same light, we recognize the role of innate immunity and inflammation in neurological development, homeostasis, and acute injury of the CNS as an exciting area with significant potential for therapeutic intervention. For this purpose, we encourage studies in models relevant to the area that will contribute to the improvement of treatments for related neurological diseases.
While innate immune mechanisms act diversely in the CNS on a range of glial cells to influence homeostasis, injury and disease; the molecules and cells employed by the innate arm may function in the CNS to modulate neural function without causing innate immune responses. At this immunologically privileged site, neuro-innate signaling may perform neurophysiological functions when neuroinflammation is absent, but confer neuropathological activities when neuroinflammation is present. We hope this topic will harness an appreciation of innate neuro-immune signaling in the CNS and its influence on neurological outcomes throughout injury and disease. We aim to capture the most recent advances and understandings of innate neuro-immune signaling during development, homeostasis, injury and developmental disorders of the CNS.
We welcome the submission of Original Research, Review, and Opinion articles covering, but not limited to, the following topics:
1. New molecular mechanisms of innate neuro-immune interaction following sterile injury, traumatic brain injury (TBI), hypoxia/ischemia, or developmental disorders.
2. Age-related differences in innate neuro-immune signaling following sterile injury, TBI, ischemia, and hypoxia.
3. Role of innate immune-glial cell interaction in blood-brain barrier (BBB) integrity and dysfunction following injury.
4. Gender differences in innate neuro-immune signaling in developmental disorders including Autism spectrum disorder (ASD), and cerebral palsy.
5. Age-related differences in innate neuro-immune signaling during the onset, development and maintenance of sterile injuries of the CNS (can include spinal cord injury).
6. New molecular mechanisms of innate component activation and signaling in the CNS during injury (i.e. via cytokines, PRRs, TLRs, inflammasomes, complement, microRNAs).
However, it is increasingly evident that similar innate immune signaling activities can have either a physiological or pathological role during development, homeostasis and acute injury in the CNS. For instance, signaling by complement and TGFβ guides both the synaptic pruning by microglia during development and the downregulation of this process in the healthy adult brain. Similarly, the IL-1 family cytokine, IL-33, which is secreted by neurons directs microglia to promote neuronal spine plasticity to aid memory consolidation. However, excessive pruning in response to IL-33 causes neuronal damage associated with schizophrenia.
There is a growing interest in the role of inflammatory cytokines (i.e. IL-1β) and inflammasomes in brain development and injury including hypoxia and ischemia. Intriguingly, cell-type-specific IL-1 receptor1 (IL-1R1) signaling in the CNS guides distinct neuronal functions and behavioral responses. Targeting this part of innate immunity has heralded great therapeutic promise in the neurodegenerative space. In the same light, we recognize the role of innate immunity and inflammation in neurological development, homeostasis, and acute injury of the CNS as an exciting area with significant potential for therapeutic intervention. For this purpose, we encourage studies in models relevant to the area that will contribute to the improvement of treatments for related neurological diseases.
While innate immune mechanisms act diversely in the CNS on a range of glial cells to influence homeostasis, injury and disease; the molecules and cells employed by the innate arm may function in the CNS to modulate neural function without causing innate immune responses. At this immunologically privileged site, neuro-innate signaling may perform neurophysiological functions when neuroinflammation is absent, but confer neuropathological activities when neuroinflammation is present. We hope this topic will harness an appreciation of innate neuro-immune signaling in the CNS and its influence on neurological outcomes throughout injury and disease. We aim to capture the most recent advances and understandings of innate neuro-immune signaling during development, homeostasis, injury and developmental disorders of the CNS.
We welcome the submission of Original Research, Review, and Opinion articles covering, but not limited to, the following topics:
1. New molecular mechanisms of innate neuro-immune interaction following sterile injury, traumatic brain injury (TBI), hypoxia/ischemia, or developmental disorders.
2. Age-related differences in innate neuro-immune signaling following sterile injury, TBI, ischemia, and hypoxia.
3. Role of innate immune-glial cell interaction in blood-brain barrier (BBB) integrity and dysfunction following injury.
4. Gender differences in innate neuro-immune signaling in developmental disorders including Autism spectrum disorder (ASD), and cerebral palsy.
5. Age-related differences in innate neuro-immune signaling during the onset, development and maintenance of sterile injuries of the CNS (can include spinal cord injury).
6. New molecular mechanisms of innate component activation and signaling in the CNS during injury (i.e. via cytokines, PRRs, TLRs, inflammasomes, complement, microRNAs).
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