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. 2021 Dec 1;143(2):179–224. doi: 10.1007/s00401-021-02384-2

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© The Author(s) 2021

Open AccessThis article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 3 — Roles of monocytes and microglia in ischemic stroke. In stroke, microglia migrate towards neurons with high intracellular calcium levels to reduce excitotoxicity and neuronal damage. Microglia also prevent bystander tissue damage by inhibiting reactive astrocytes and phagocytosing infiltrating neutrophils. CXCR4⁺ MDM are recruited to the site of injury, where they produce microglia-activating mediators, IL-1β and ROS, and stimulate microglia proliferation and the glial scar formation. These inflammatory mediators may also injure neurons and contribute to secondary damage. CNS-infiltrating Ly6C^hi monocytes may also help repair the damaged BBB via the production of collagen-4 and TGF-β1. BBB, blood–brain barrier; CXCR4, CXC chemokine receptor type 4; CXCL12, CXC Motif Chemokine Ligand 12; IL, interleukin; MDM, monocyte-derived macrophage; ROS, reactive oxygen species; TGF-β1, transforming growth factor beta 1