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. 2021 Jun 10;19:254. doi: 10.1186/s12967-021-02922-2

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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. 3 — The interaction between the mesenteric lymphatics and the intestinal flora. Invading intestinal mucosal bacteria interact with various immune cells in mesenteric lymph nodes, such as T cells, B cells, DC cells, macrophages, NK cells, and neutrophils. When bacteria stimulate the mesenteric lymph nodes, more IFN-C is secreted. At the same time, bifidobacteria can lead to decreased IL-6, TNF-α, and IL-12 secretion of DC cells. Also, the presence of microorganisms can activate the CD40 pathway and make CD103+ cells migrate from lamina propria to MLN, playing an important role in immune regulation, hence lymphangiogenesis