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. 2021 Sep 16;18:206. doi: 10.1186/s12974-021-02263-3

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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. 6 — Microglial activation in DBA/2J retina was inhibited after 1,25(OH)₂D₃ treatment. Upper panel shows representative images of microglial activation evaluated by immunohistochemistry with the Iba-1 marker in control (vehicle-treated) and 1,25(OH)₂D₃-treated groups. Scale bar, 50 μm. The density of activated microglial cells was calculated by counting the number of Iba-1⁺ cells normalized to the scanned area. The quantification was carried out on whole retina (A), on both retinal centre and periphery (B). Data are plotted as mean ± SD (n = 6 flat-mount retinas for each experimental group, n = 48 images for each experimental group): A *p = 0.0400 vs. Ctrl, t-test two-tailed. B *p = 0.0186 vs. Ctrl periphery (Ctrl p) ^‡p = 0.0186 vs. Ctrl centre (Ctrl c), one-way ANOVA with Tukey post hoc test for multiple comparison