Major cellular populations and representative state tendencies in the neuroimmune environment.
| Cell type | Primary physiological functions | Representative molecular markers | Role in CNS homeostasis | Representative roles during neurological disease |
|---|---|---|---|---|
| Microglia | Immune surveillance, phagocytosis of apoptotic cells and debris, synaptic remodeling, regulation of neuronal activity | P2RY12, CX3CR1, TMEM119 | Continuous monitoring of the neural microenvironment, maintenance of synaptic integrity, clearance of damaged cellular components [21] | Context-dependent shifts toward inflammatory, phagocytic, metabolic, repair-associated, or disease-associated programs, including TREM2-associated responses to lipid-rich debris, amyloid pathology, and neurodegenerative tissue damage [21, 22] |
| Astrocytes | Regulation of neurotransmitter levels, metabolic support for neurons, potassium buffering, neurovascular coupling | S100β, AQP4, GLAST/EAAT1; GFAP in reactive states or selected astrocyte populations | Maintenance of extracellular ion balance, modulation of synaptic transmission, metabolic support of neurons, regulation of blood-brain barrier stability [8, 23] | Context-dependent astrocyte remodeling programs that may support neuroprotection, inflammatory signaling, synaptic dysfunction, barrier regulation, scar formation, or tissue remodeling depending on timing and disease context [24] |
| Neural stem cells | Generation of neurons and glial cells, maintenance of neurogenic niches, contribution to neural plasticity | SOX2, Nestin, GFAP (subset), DCX (progenitors) | Maintenance of quiescent stem-cell pools and controlled neurogenesis within specialized niches such as the subventricular zone and dentate gyrus [25, 26] | Altered activation, proliferation, and lineage decisions in response to inflammatory signaling, injury, or neurodegenerative conditions [27] |
| Endothelial cells | Formation of the blood-brain barrier, regulation of molecular transport, vascular signaling | Claudin-5, VE-cadherin, PECAM-1, GLUT1 | Maintenance of vascular integrity and selective permeability between the systemic circulation and neural tissue [28, 29] | Barrier dysfunction, increased permeability, and recruitment of immune cells during neuroinflammatory and neurodegenerative disorders [29] |
| Pericytes | Structural support of microvessels, regulation of vascular stability and permeability | PDGFRβ, NG2, CD146 | Stabilization of capillary structure and maintenance of blood-brain barrier function [28, 30] | Vascular dysregulation and blood-brain barrier disruption contributing to inflammation and neurodegeneration [30] |
| Peripheral immune cells | Systemic immune surveillance and inflammatory signaling | CD45, CD3 (T cells), CD68 (macrophages), Ly6G (neutrophils) | Limited immune monitoring under tightly regulated vascular control [15, 31] | Infiltration into the CNS during pathological conditions, contributing to inflammatory signaling, tissue damage, or repair responses [31] |
Note: The markers and functions listed in this table are representative rather than exhaustive. Cellular states in the central nervous system exist along dynamic continua that vary according to developmental stage, anatomical region, disease context, species, timing of injury, and local microenvironment. Therefore, the listed markers should not be interpreted as defining fixed cellular identities, and the disease-associated roles should be viewed as context-dependent state tendencies rather than mutually exclusive or stable phenotypes.
MMN: Conceptualization, Methodology, Investigation, Resources, Data curation, Formal analysis, Visualization, Writing—original draft, Writing—review & editing. The author read and approved the submitted version.
The author declares no conflicts of interest.
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