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. 2023 Oct 13;15(6):2507–2525. doi: 10.14336/AD.2023.1010

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Copyright: © 2024 Wang et al.

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Figure 4. — Crosstalk between glial cells and peripheral immune cells regulating BBB integrity after AIS. (A) Pro-inflammatory cytokines promote interaction and polarization between Th1 and M1 microglia, causing BBB injury. Double-negative T cells (DNT) increase the number of M1 microglia via the Fas ligand/protein tyrosine phosphatase non-receptor type 2/tumor necrosis factor-α pathway. M1 microglia enhance CD8⁺T activity by secreting interleukin-15 (IL-15), and conversely, CD8⁺T cell induces cytotoxicity via granzyme-b and tumor necrosis factor-α (TNF-α), enhancing stroke progression. NK cells can damage BBB via interferon-inducible protein-10 (IP-10). Reactive oxygen species (ROS) and peptidylarginine deiminase 4 (PAD4) stimulate neutrophils to produce neutrophil extracellular traps (NETs) and astrocytes to secrete pro-inflammatory cytokines, such as IL-15 and interleukin-17A (IL-17A) and secrete chemokines to promote the recruitment of CD8⁺T cells, NK cells and B cells, resulting in BBB damage. (B) Treg enhances tight junctions (TJPs) of BBB and protection by both inhibiting M1 microglia polarization and enhancing TJP expression. Th2 protects the BBB by promoting M2 microglia polarization with inhibition of NF-κB and NLRP3-mediated inflammatory responses. B cells inhibit the post-ischemic response of M1 microglia with Treg. Cytokines C-X-C motif chemokine ligand 2 (CXCL2) and fibroblast growth factors 1 (FGF1) are upregulated in Treg-stimulated microglia, promote Treg-microglia interaction and oligodendrogenesis, and promote white matter repair, thereby protecting the BBB.