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. 2018 Dec 7;8:17727. doi: 10.1038/s41598-018-36012-z

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© The Author(s) 2018

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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Blocking LT-LTβR signaling enhances Th1 response by up-regulating IL-12 expression from monocyte-derived cells. (a) Expression of IL-12 in the popliteal LN of LysM^ΔLtbr mice on day 4 p.i. (n = 5/group). (b,c) Th1 response of LysM^ΔLtbr mice on day 14 p.i. (n = 4/group). Immunospots (b), and absolute number of IFNγ-secreting CD4⁺ cells per LN (c). Data are representative of three independent experiments, shown as mean ± SEM. n.s., not significant; *P < 0.05; **P < 0.01; ***P < 0.001. (Two-tailed paired Student’s t test for a,c).