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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 over-production of IL-12. (a) IFNγ secretion in the popliteal LN from WT mice (solid line) and LTβR-Ig-treated mice (dotted line) detected by CBA test (n = 5/group). (b) IL-12 secretion in the popliteal LN from WT mice (solid line) and LTβR-Ig-treated mice (dotted line) detected by CBA test (n = 5/group). (c) Anti-IFNγ (clone XMG1.2, 500 μg/mouse) was i.p. administered every third day from the day before HSV-1 infection. Th1 response was detected on day 14 p.i. by Elispot (n = 4/group). Immunospots and absolute numbers of IFNγ-secreting CD4⁺ cells per LN are shown. (d) Anti-IL-12p75 (clone R5-9A2, 500 μg/mouse) was i.p. injected every third day from the day before HSV-1 infection. Th1 response was detected on day 14 p.i. by Elispot (n = 4/group). Immunospots and absolute numbers of IFNγ-secreting CD4⁺ cells per LN are shown. 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-way ANOVA multiple comparisons for a,b).