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. 2022 Jun 6;19:132. doi: 10.1186/s12974-022-02492-0

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© The Author(s) 2022

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/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 2 — Microglial M1/M2 polarization and their regulatory functions in the CNS. Resting microglia are stimulated with pathogen-associated molecular patterns (PAMPs) or danger-associated molecular patterns (DAMPs) via toll-like receptors (TLRs). In the presence of lipopolysaccharide (LPS) and interferon-γ (IFN-γ), microglia polarize to the M1 phenotype and produce pro-inflammatory mediators including interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), CCL2, reactive oxygen species (ROS), and NO. In contrast, IL-4, IL-13, or IL-10 cause alternative activation into M2 microglia that inhibit M1 functions by releasing anti-inflammatory cytokines and neurotrophic factors [40]