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. 2021 Apr 19;18:94. doi: 10.1186/s12974-021-02147-6

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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/. 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. 5 — Human PSC-derived microglia show elevated cell death when treated with media from human PSC-derived striatal neurons expressing mutant HTT with a long polyglutamine-tract. IsoHD PSC-derived microglia were cultured with supernatants harvested from IsoHD PSC-derived striatal neurons. a Exposure to supernatants from untreated neuronal cultures for five days did not reveal any HTT polyglutamine-dependent effects, either of the donor neurons or the recipient microglia, on LDH release by the microglia. b By contrast, when the neurons had been heat-shocked at 45 °C for 45 min to induce stress, recipient microglia of all HTT genotypes showed elevated LDH release when treated with supernatants from HTT 80^Q neurons compared with those from the 30^Q and 45^Q ones. Data are presented as mean ± SEM, n = 3, analysed by two-way ANOVA with Tukey’s multiple comparisons test