ReviewNeurochemical research2026
Bidirectional Regulatory Mechanisms of T cell-microglia Interactions in Cerebral Ischemic Disease: Molecular Crosstalk, Experimental Techniques and Therapeutic Implications.
Review in Neurochemical research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Authors and funding
15 authors.
Funding
Abstract
Cerebral ischemic diseases, such as ischemic stroke (IS) and vascular dementia (VaD), are major causes of neurological disability and mortality. Neuroinflammation acts as a pivotal driver of secondary brain injury, mediated by intricate bidirectional interactions between peripheral T cells and central nervous system (CNS)-resident microglia. This review delineates the molecular mechanisms underlying T cell-microglia crosstalk in cerebral ischemia, emphasizing their dual roles in exacerbating neurotoxicity and promoting repair. Direct interactions involve antigen presentation via MHC-TCR engagement and co-stimulatory checkpoints (e.g., CD80/CD86-CD28, PD-L1-PD-1), which regulate T cell activation and microglial polarization. Direct signaling through cytokines (IFN-γ, IL-4, IL-17, IL-10) further modulates microglial phenotypes: Th1/Th17 cells drive pro-inflammatory M1 polarization via STAT1/NF-κB pathways, while Tregs/Th2 cells induce anti-inflammatory M2 states through STAT6/SMAD signaling. Spatial transcriptomics and single-cell omics reveal spatiotemporal dynamics of these interactions, identifying STAT1/STAT6 imbalance as a critical determinant of neuroinflammatory outcomes. Advanced methodologies, including two-photon intravital microscopy and microfluidic blood-brain barrier (BBB) models, enable real-time visualization of immune cell trafficking and synaptic communication. Therapeutically, targeting immune checkpoints (CTLA-4, PD-1) or cytokine pathways (e.g., IL-4 mimetics) shows promise in recalibrating neuroimmune responses. However, challenges such as blood-brain barrier impermeability to biologics and interspecies immune heterogeneity necessitate innovative delivery strategies. This review integrates molecular, cellular, and technological insights to propose a framework for precision immunomodulation. By elucidating context-dependent signaling nodes and leveraging emerging tools, the study underscores the potential of harnessing T cell-microglia crosstalk to mitigate neuroinflammation and enhance neural repair, offering transformative avenues for stroke and dementia therapy.
Indexed as
Identifiers
42900246What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.