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The Role of Intestinal Epithelial Cell Signaling In Mucosal Immunity

Received: 22 November 2022     Accepted: 3 January 2023     Published: 10 January 2023
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Abstract

In the words of Hippocrates, all disease begin in the gut. In the intestinal lumen, there are more than 1000 species of microbiota members containing 600,000 genes. that is 10 times more than the number of nucleated cells in our body. Connections such as tight junction (TJ) and adherens junction (AJ) between epithelial cells prevent the passage of microorganisms and antigens to the lamina proprea, while transmitting the received stimuli with signaling mechanisms. Integrin and immunoglobulin like adhesion molecules, which are members of the tight junction, receive signaling with ErbB (Her1, EGFR/2/3) and cytokine receptors (transforming growth factor TGFβ receptors) and transmit them to the nucleus, creating signals for gene transcription, proliferation, differentiation, cytokine synthesis, synthesis of surface receptors, epithelial mesenchimal transition (Emt) regulation, or apoptosis and growth arrest. Tight junction transmembrane proteins, scaffolding proteins such as zonulin, communicate with afadin-mediated AJ, allowing signals to be transmitted to the cytoskeleton. It makes gene expression with the transcription factor to which it is attached. It contributes to the ion balance with claudin, cytoskeleton regulation with occludin, gene transcription and cytokine synthesis with Marveld3, from the members of the TAMPs family to which it is linked. The stimulated cell synthesizes Wingless-ınt1 (Wnt) signaling molecules and performs paracrine and autocrine signaling. It balances intracellular Ca+2 level with non-canonical Wnt pathway, provides cell polarity especially via Cell division control protein 42 (CDC42) with non-canonical polarity pathway, β-catenin mediated gene transcription with canonical Wnt pathway. While microbial antigens are recognized by Toll like receptors (TLR) and cytokines are synthesized, antigen molecule presentation is regulated by major histocompatibility complex (Mhc) molecules. Cytokines synthesized by signaling trigger innate immunity in the lamina propria (LP) and adaptive immunity consisting of 50x109 lymphocytis, thereby initiating the anti-inflammatory or pro-inflammatory process. This review describes all these mechanisms and their connections.

Published in Cell Biology (Volume 10, Issue 2)
DOI 10.11648/j.cb.20221002.11
Page(s) 41-52
Creative Commons

This is an Open Access article, distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution and reproduction in any medium or format, provided the original work is properly cited.

Copyright

Copyright © The Author(s), 2023. Published by Science Publishing Group

Keywords

Tight Junction, Zonulin, CDC42, Gut Homing, B1 Lymphocytes

References
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    Meral Simsek. (2023). The Role of Intestinal Epithelial Cell Signaling In Mucosal Immunity. Cell Biology, 10(2), 41-52. https://doi.org/10.11648/j.cb.20221002.11

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    Meral Simsek. The Role of Intestinal Epithelial Cell Signaling In Mucosal Immunity. Cell Biol. 2023, 10(2), 41-52. doi: 10.11648/j.cb.20221002.11

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    Meral Simsek. The Role of Intestinal Epithelial Cell Signaling In Mucosal Immunity. Cell Biol. 2023;10(2):41-52. doi: 10.11648/j.cb.20221002.11

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  • @article{10.11648/j.cb.20221002.11,
      author = {Meral Simsek},
      title = {The Role of Intestinal Epithelial Cell Signaling In Mucosal Immunity},
      journal = {Cell Biology},
      volume = {10},
      number = {2},
      pages = {41-52},
      doi = {10.11648/j.cb.20221002.11},
      url = {https://doi.org/10.11648/j.cb.20221002.11},
      eprint = {https://article.sciencepublishinggroup.com/pdf/10.11648.j.cb.20221002.11},
      abstract = {In the words of Hippocrates, all disease begin in the gut. In the intestinal lumen, there are more than 1000 species of microbiota members containing 600,000 genes. that is 10 times more than the number of nucleated cells in our body. Connections such as tight junction (TJ) and adherens junction (AJ) between epithelial cells prevent the passage of microorganisms and antigens to the lamina proprea, while transmitting the received stimuli with signaling mechanisms. Integrin and immunoglobulin like adhesion molecules, which are members of the tight junction, receive signaling with ErbB (Her1, EGFR/2/3) and cytokine receptors (transforming growth factor TGFβ receptors) and transmit them to the nucleus, creating signals for gene transcription, proliferation, differentiation, cytokine synthesis, synthesis of surface receptors, epithelial mesenchimal transition (Emt) regulation, or apoptosis and growth arrest. Tight junction transmembrane proteins, scaffolding proteins such as zonulin, communicate with afadin-mediated AJ, allowing signals to be transmitted to the cytoskeleton. It makes gene expression with the transcription factor to which it is attached. It contributes to the ion balance with claudin, cytoskeleton regulation with occludin, gene transcription and cytokine synthesis with Marveld3, from the members of the TAMPs family to which it is linked. The stimulated cell synthesizes Wingless-ınt1 (Wnt) signaling molecules and performs paracrine and autocrine signaling. It balances intracellular Ca+2 level with non-canonical Wnt pathway, provides cell polarity especially via Cell division control protein 42 (CDC42) with non-canonical polarity pathway, β-catenin mediated gene transcription with canonical Wnt pathway. While microbial antigens are recognized by Toll like receptors (TLR) and cytokines are synthesized, antigen molecule presentation is regulated by major histocompatibility complex (Mhc) molecules. Cytokines synthesized by signaling trigger innate immunity in the lamina propria (LP) and adaptive immunity consisting of 50x109 lymphocytis, thereby initiating the anti-inflammatory or pro-inflammatory process. This review describes all these mechanisms and their connections.},
     year = {2023}
    }
    

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    AU  - Meral Simsek
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    AB  - In the words of Hippocrates, all disease begin in the gut. In the intestinal lumen, there are more than 1000 species of microbiota members containing 600,000 genes. that is 10 times more than the number of nucleated cells in our body. Connections such as tight junction (TJ) and adherens junction (AJ) between epithelial cells prevent the passage of microorganisms and antigens to the lamina proprea, while transmitting the received stimuli with signaling mechanisms. Integrin and immunoglobulin like adhesion molecules, which are members of the tight junction, receive signaling with ErbB (Her1, EGFR/2/3) and cytokine receptors (transforming growth factor TGFβ receptors) and transmit them to the nucleus, creating signals for gene transcription, proliferation, differentiation, cytokine synthesis, synthesis of surface receptors, epithelial mesenchimal transition (Emt) regulation, or apoptosis and growth arrest. Tight junction transmembrane proteins, scaffolding proteins such as zonulin, communicate with afadin-mediated AJ, allowing signals to be transmitted to the cytoskeleton. It makes gene expression with the transcription factor to which it is attached. It contributes to the ion balance with claudin, cytoskeleton regulation with occludin, gene transcription and cytokine synthesis with Marveld3, from the members of the TAMPs family to which it is linked. The stimulated cell synthesizes Wingless-ınt1 (Wnt) signaling molecules and performs paracrine and autocrine signaling. It balances intracellular Ca+2 level with non-canonical Wnt pathway, provides cell polarity especially via Cell division control protein 42 (CDC42) with non-canonical polarity pathway, β-catenin mediated gene transcription with canonical Wnt pathway. While microbial antigens are recognized by Toll like receptors (TLR) and cytokines are synthesized, antigen molecule presentation is regulated by major histocompatibility complex (Mhc) molecules. Cytokines synthesized by signaling trigger innate immunity in the lamina propria (LP) and adaptive immunity consisting of 50x109 lymphocytis, thereby initiating the anti-inflammatory or pro-inflammatory process. This review describes all these mechanisms and their connections.
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Author Information
  • Department of Pediatrics, Gulhane Faculty of Medicine, Ankara, Turkey

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