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Pathogen adhesion sites on epithelial cells are not a single, well-defined molecular target but rather a functional category referring to multiple host cell surface molecules and complexes (such as glycoproteins, glycolipids, cadherins, selectins, integrins, and other adhesion molecules) that can be exploited by bacterial, viral, or parasitic pathogens for attachment and entry into epithelial tissues[1][2][3][5]. Pathogens use specialized adhesins, pili, or secretion systems to recognize and bind these host molecules, which enables colonization and can facilitate invasion, barrier disruption, and host infection[1][2][4][5]. These sites include, but are not limited to, lectin-binding carbohydrates, proteins like E-cadherin, nectins, selectins, integrins, and newly discovered targets such as Clec2e[5]. Because this is a broad descriptive category rather than a specific molecular entity, it is not considered a canonical "therapeutic target" in the strict sense, and strategies to prevent pathogen adhesion typically focus on blocking multiple types of interactions or the pathogen’s adhesins, not a single defined receptor or molecule on the host side[1][2][5].
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