以色列魏茨曼科学研究所Ranit Kedmi课题组的一项最新研究开发出协调的细胞网络调节对食物的耐受性。2025年5月27日出版的《自然》发表了这项成果。

然而，该研究团队现在报道了食物特异性pTreg细胞完全由最近鉴定的RORγt APCs4-8诱导，而不是由cDC诱导。相反，他们的数据表明，pTreg-cDC1在稳态下的相互作用限制了食物特异性CD8αβ T细胞的扩增。在感染或食物中毒期间，这种调节被打破，使饮食中的CD8αβ T细胞能够扩增并获得对模拟食物抗原的效应功能。与典型感染不同的是，在病原体被清除后，饮食中的CD8αβ T细胞不会对其相应的饮食抗原做出反应而扩增。

因此，该研究团队提出，在对膳食抗原的反应中，耐受是由专用抗原呈递细胞（APCs）和T细胞组成的回路介导的。当宿主受到感染挑战时，该回路允许保护效应反应的短暂扩展，而不会损害确保安全食品消费的总体耐受策略。

研究人员表示，为了吸收营养和支持共生微生物，宿主通过外周调节性T细胞（pTregs）诱导耐受性免疫反应。先前的研究发现，1型树突状细胞（cDC1）是膳食pTregs的启动物。

附：英文原文

Title: A coordinated cellular network regulates tolerance to food

Author: Rudnitsky, Anna, Oh, Hanna, Margolin, Maya, Dassa, Bareket, Shteinberg, Inbar, Stoler-Barak, Liat, Shulman, Ziv, Kedmi, Ranit

Issue&Volume: 2025-05-27

Abstract: To absorb nutrients and support commensal microbes, the host induces tolerogenic immune responses via peripheral regulatory T cells (pTregs) 1,2. Prior studies identified type 1 dendritic cells (cDC1) as initiators of dietary pTregs3. However, we now report that food-specific pTreg cells are exclusively induced by the recently identified RORγt APCs4–8 and not by cDCs. Instead, our data suggest that pTreg–cDC1 interactions in steady-state limit the expansion of food-specific CD8αβ T cells. This regulation breaks during infection or food poisoning, enabling dietary CD8αβ T cells to expand and acquire effector functions in response to mimicked food antigens. Unlike in typical infections, after the pathogen is cleared, dietary CD8αβ T cells do not expand in response to their corresponding dietary antigens. Thus, we propose that in response to dietary antigens, tolerance is mediated by a circuit of dedicated antigen-presenting cells (APCs) and T cells. When the host is challenged by infection, this circuit permits the transient expansion of protective effector responses without compromising the overall strategy of tolerance that ensures safe food consumption.

DOI: 10.1038/s41586-025-09173-x

Source: https://www.nature.com/articles/s41586-025-09173-x