Autophagy, viruses, and intestinal immunity.
Autophagy, viruses, and intestinal immunity.
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DOI：
10.1097/mog.0000000000000121
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发表时间：
2014-11
影响因子：
2.5
通讯作者：
Cadwell K
中科院分区：
文献类型：
--
作者：
Kernbauer E;Cadwell K
强调最近的发现，确定自噬的细胞降解途径在控制对肠道病原体和共生体的平衡反应中起着至关重要的作用。随着自噬与炎症性肠病(IBD)易感性的遗传关联，越来越多的证据表明，这一途径在各种上皮谱系中发挥作用，以支持肠道屏障。新的研究也揭示了自噬蛋白决定了免疫反应的质量和大小。特别是小鼠模型表明，自噬和IBD易感基因调节对病毒的炎症反应，这一发现与越来越多的人认识到病毒与宿主和微生物区系之间的复杂相互作用超出了明显的宿主-病原体关系。自噬和其他免疫或应激反应途径在粘膜免疫中相交，决定了对病原体和共生性病原体的反应。对胃肠道疾病的新治疗策略以及预后和诊断工具的开发将极大地促进对这些相互作用的深入了解，这些相互作用以细胞类型和微生物特有的方式，包括微生物群中较少被认识的成分，如真核和原核病毒。
To highlight recent findings that identify an essential role for the cellular degradative pathway of autophagy in governing a balanced response to intestinal pathogens and commensals. Following the genetic association of autophagy with inflammatory bowel disease (IBD) susceptibility, increasing evidence indicate that this pathway functions in various epithelial lineages to support the intestinal barrier. New studies are also revealing that autophagy proteins dictate the quality and magnitude of immune responses. Mouse models in particular suggest that autophagy and IBD susceptibility genes regulate inflammatory responses to viruses, a finding that coincides with an increasing appreciation that viruses have intricate interactions with the host and the microbiota beyond the obvious host-pathogen relationship. Autophagy and other immunological or stress response pathways intersect in mucosal immunity to dictate the response to pathogenic and commensal agents. The development of novel treatment strategies as well as prognostic and diagnostic tools for gastrointestinal disorders will be greatly facilitated by a deeper understanding of these interactions at the cell type and microbe-specific manner, which includes less appreciated components of the microbiota such as eukaryotic and prokaryotic viruses.