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. 2018 Dec 21;10(1):11. doi: 10.1038/s41419-018-1240-3

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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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Fig. 7 — CCR4 regulates the magnitude of pulmonary inflammation at the chronic phase of M. tuberculosis infection by a mechanism dependent on the balance in the ratio of CD4⁺Foxp3⁺regulatory T cells and CD4⁺ Th1 effector cells, as well as in the suppressor function of regulatory T cells. Consequently, CCR4 deficiency accentuates the susceptibility to infection by a mechanism dependent on exacerbated magnitude of Th1 cell-mediated pulmonary inflammation