上皮源性白介素23促进口腔黏膜免疫病理发生，这一成果由美国国立卫生研究院Niki M. Moutsopoulos研究小组取得。这一研究成果于2024年3月20日发表在国际顶尖学术期刊《免疫                                                                                                         》上。

该课题组人员证明上皮细胞内产生的白介素23(IL-23)在流行的口腔疾病牙周炎中引发炎症循环。上皮IL-23的表达定位于疾病相关微生物组的近端区域，并且在实验模型和常见和遗传形式的疾病患者中很明显。

在机制上，牙周炎微生物组的鞭毛微生物以TLR5受体依赖的方式引起上皮IL-23诱导。因此，与其他Th17驱动的疾病不同，非造血细胞来源的IL-23作为牙周炎致病性炎症的起始因子。除牙周炎外，对公开数据集的分析显示上皮IL-23在感染、恶性肿瘤和自身免疫环境中的表达，表明上皮内IL-23在人类疾病中具有更广泛的作用。

总的来说，这项工作强调了屏障上皮在诱导IL-23介导的炎症中的重要作用。

据悉，在粘膜表面，上皮细胞提供结构屏障和免疫防御系统。然而，失调的上皮反应可能导致疾病状态。

附：英文原文

Title: Epithelial-derived interleukin-23 promotes oral mucosal immunopathology

Author: Tae Sung Kim, Tomoko Ikeuchi, Vasileios Ionas Theofilou, Drake Winslow Williams, Teresa Greenwell-Wild, Armond June, Emmanuel E. Adade, Lu Li, Loreto Abusleme, Nicolas Dutzan, Yao Yuan, Laurie Brenchley, Nicolas Bouladoux, Yosuke Sakamachi, Robert J. Palmer, Ramiro Iglesias-Bartolome, Giorgio Trinchieri, Stavros Garantziotis, Yasmine Belkaid, Alex M. Valm, Patricia I. Diaz, Steven M. Holland, Niki M. Moutsopoulos

Issue&Volume: 2024-03-20

Abstract: At mucosal surfaces, epithelial cells provide a structural barrier and an immune defensesystem. However, dysregulated epithelial responses can contribute to disease states.Here, we demonstrated that epithelial cell-intrinsic production of interleukin-23(IL-23) triggers an inflammatory loop in the prevalent oral disease periodontitis.Epithelial IL-23 expression localized to areas proximal to the disease-associatedmicrobiome and was evident in experimental models and patients with common and geneticforms of disease. Mechanistically, flagellated microbial species of the periodontitismicrobiome triggered epithelial IL-23 induction in a TLR5 receptor-dependent manner.Therefore, unlike other Th17-driven diseases, non-hematopoietic-cell-derived IL-23served as an initiator of pathogenic inflammation in periodontitis. Beyond periodontitis,analysis of publicly available datasets revealed the expression of epithelial IL-23in settings of infection, malignancy, and autoimmunity, suggesting a broader rolefor epithelial-intrinsic IL-23 in human disease. Collectively, this work highlightsan important role for the barrier epithelium in the induction of IL-23-mediated inflammation.

DOI: 10.1016/j.immuni.2024.02.020

Source: https://www.cell.com/immunity/abstract/S1074-7613(24)00096-7