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. 2013 Sep 17;4:280. doi: 10.3389/fimmu.2013.00280

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Copyright © 2013 Pastorelli, De Salvo, Mercado, Vecchi and Pizarro.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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The intestinal epithelial barrier plays a central role in gut homeostasis. IECs form an semi-permeable lining, with barrier function modulated by the presence of TJs, AJs, and desmosomes. Expression and assembly of these protein complexes are finely regulated by several intracellular pathways. Polymorphisms in MYO9B, PARD3, and MAGI2 and impairment of the Gαi2/adenylate cyclase axis result in defective TJ assembly; phosphorylation of myosin II through MLCK activation by TNF leads to TJ disassembly. Lack of junctional proteins, such as JAM-A, or altered expression and/or pairing (e.g., dominant negative N-cadherin, claudin-2 overexpression) leads to increased epithelial permeability, facilitating translocation of luminal bacteria, and antigens and exposure to the mucosal adaptive immune system.