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. 2017 May 31;8:15648. doi: 10.1038/ncomms15648

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Copyright © 2017, The Author(s)

Open Access This 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 license, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/

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(a) The experimental set-up to test the role of CD91⁺ DCs in HSP-mediated immune-regulatory response. Immunization was carried out using irradiated D122 (Groups 1 and 3) or control PBS (Group 2). Suppression of anti-tumour immunity, primed by irradiated D122, was mediated by high-dose (HD) gp96 treatment (Group 3) or control PBS (Groups 1 and 2). All mice were challenged with D122 and tumour growth was monitored. (b) Tumour growth in wild-type littermates (CD91^f/f). (c) Tumour growth in mice lacking expression of CD91 in CD11c⁺ cells (CD91^f/fCD11^cre). Shown is the average tumour diameter ± s.e.m. n=3–5/group, data are from one representative experiment of three independent experiments. (The value of s.e.m. in Group 3 is too small to be seen in the graph). Data are represented as mean±s.e.m. ns not significant, *P<0.05 versus control (area under curve).