Neuron Immune Crosstalk
Neuron Immune Crosstalk - Related Videos
01:38
What is the Immune System?
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2019
Overview The immune system comprises diverse biological structures and processes that protect the body from disease. These processes can be classified into innate and adaptive immunity. To work effectively, the immune system needs to detect pathogens by distinguishing the body’s own structures from foreign elements. If this determination fails, autoimmune diseases occur in which the immune system reacts against the body’s own tissue. The Innate Immune System Acts Fast and Non-specifically
07:41
Establishing Mixed Neuronal and Glial Cell Cultures from Embryonic Mouse Brains to Study Infection and Innate Immunity
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Cited by 2 •
2023
This protocol presents a unique way of generating central nervous system cell cultures from embryonic day 17 mouse brains for neuro(immuno)logy research. This model can be analyzed using various experimental techniques, including RT-qPCR, microscopy, ELISA, and flow cytometry.
07:36
Contact-Free Co-Culture Model for the Study of Innate Immune Cell Activation During Respiratory Virus Infection
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Cited by 1 •
2021
This protocol details an investigation of the early interactions between virally infected nasal epithelial cells and innate cell activation. Individual subsets of immune cells can be distinguished based on their activation in response to viral infections. They can then be further investigated to determine their effects on early antiviral responses.
08:32
Engineering Tendon Assembloids to Probe Cellular Crosstalk in Disease and Repair
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Cited by 4 •
2024
Here, we present an assembloid model system to mimic tendon cellular crosstalk between the load-bearing tendon core tissue and an extrinsic compartment containing cell populations activated by disease and injury. As an important use case, we demonstrate how the system can be deployed to probe disease-relevant activation of extrinsic endothelial cells.
05:07
Isolation, Characterization and Functional Examination of the Gingival Immune Cell Network
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Cited by 34 •
2016
We have established a technique for the isolation, phenotypic characterization and functional analysis of immune cells from murine gingiva.
FAQs
Outcomes depend on which neuron- or immune-cell receptor recognizes the opposing cell’s signal. Neurotransmitters and neuropeptides can alter immune-cell behavior, whereas cytokines and related immune mediators can change neuronal excitability or synaptic function. Consequently, the same communication network may produce different effects depending on the signals released and the receptors available, rather than acting as a single uniform pathway.
Bidirectional signaling allows neural activity to influence immune responses while immune-derived signals feed information back to neurons. This reciprocal arrangement can coordinate defense and tissue repair with changes in neural function. It also creates opportunities for feedback: persistent immune signaling may continue affecting excitability or synapses, while neural signals may help shape ongoing immune-cell behavior.
Protection and dysfunction can arise from the same signaling capacity. During infection or injury, communication may help coordinate defense and tissue repair. If inflammatory signaling persists, however, it can sustain neuroinflammation and contribute to pain, neurodegenerative disease, or altered brain function. Examining duration and biological context therefore matters when interpreting whether a response is adaptive or harmful.
Useful readouts include changes in neuronal excitability, synaptic function, immune-cell behavior, and inflammatory signaling. Examining these outcomes together is more informative than measuring only one cell type, because crosstalk is reciprocal. In neuroscience, this combined perspective helps investigators connect an immune mediator or neural signal with functional consequences for both nervous-system activity and immune responses.
Research in this area is especially relevant when neural function changes alongside inflammation, including pain, neurodegenerative disease, and altered brain function. The framework encourages investigators to ask whether immune-derived mediators affect neuronal excitability or synapses, and whether neural signals influence immune behavior. Such questions connect cellular communication with broader disease-associated changes without treating the nervous and immune systems separately.
Potential interventions must balance two goals: reducing damaging inflammatory signaling and preserving essential neural or protective immune functions. This principle follows directly from the dual role of the communication network, which can support defense and repair yet also contribute to persistent neuroinflammation. Research can therefore evaluate whether a target changes pathological signaling selectively rather than broadly suppressing neuron-immune communication.