ArticleJournal of virology2026
PEDV regulates trans-mammary epithelial migration of T cells in a CCR10/CCL28-dependent manner.
Article in Journal of virology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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8 authors.
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Abstract
Porcine epidemic diarrhea virus (PEDV) is a re-emerging coronavirus that infects neonatal piglets via newly discovered colostrum transmission routes. Research has shown that T cells carrying PEDV in colostrum can infect piglets, but the mechanism is unclear. This study revealed that PEDV impairs T-cell immune function, preventing the production of granzymes, perforin, and interferon-γ. Furthermore, RNA sequencing of PEDV-infected and uninfected T cells revealed significant differences in gene expression: the expression of CCR10 on T-cell surfaces increased, whereas the expression of vinculin, α-actinin, paxillin, FAK, and talin-1 decreased ( IMPORTANCE: Understanding the impact of porcine epidemic diarrhea virus (PEDV) on T-cell function and migration is crucial. This study reveals PEDV impairs T-cell immunity by preventing key molecule production. It uncovers significant gene expression changes in infected T cells, with CCR10 rising and several adhesion-related proteins falling. Further, CCR10 interacts solely with CCL28, and PEDV upregulates CCL28 in PMECs, is key. The transwell system experiments show CCL28's chemotactic effect on T cells, linked to paxillin and FAK expression changes. These findings shed light on how PEDV manipulates T-cell migration via the CCR10/CCL28 axis, aiding in developing strategies against PEDV.
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