杜克大学医学院Daniel R. Saban小组的研究发现常驻组织巨噬细胞维持眼压稳态。相关论文于2026年3月9日发表在《免疫学》杂志上。

利用巨噬细胞谱系追踪方法，小组发现了巨噬细胞在整个小鼠生命周期中具有不同空间组织的双重个体发生。长寿命的常驻组织巨噬细胞主要集中在小梁网和Schlemm管中，而稳态单核细胞来源的巨噬细胞则在远端血管周围大量存在。常驻组织巨噬细胞的特异性耗竭引发眼压升高和流出阻力升高，这与小梁网产生阻力的组织中异常的细胞外基质转换有关。相反，当单核细胞来源的巨噬细胞被耗尽时，没有观察到生理失调和组织重塑。总之，该课题组人员展示了流出道内个体发生和组织特异性巨噬细胞的功能，揭示了常驻组织巨噬细胞在产生阻力的组织中的整体稳态作用，这些组织的功能障碍是导致青光眼的原因。

据介绍，眼压受到常规流出组织的严格调节，防止眼压升高导致视神经退行性变或青光眼。尽管巨噬细胞遍布常规流出道，但它们在调节眼压中的作用尚不清楚。

附：英文原文

Title: Resident tissue macrophages maintain intraocular pressure homeostasis

Author: Katy C. Liu, Aleksander O. Grimsrud, Maria Fernanda Suarez, Darren Schuman, Michael L. De Ieso, Megan Kuhn, Ruth A. Kelly, Rose Mathew, Joan Kalnitsky, Matthias Mack, Gerasimos Anagnostopoulos, Florent Ginhoux, Violet Bupp-Chickering, Revathi Balasubramanian, Simon W.M. John, W. Daniel Stamer, Daniel R. Saban

Issue&Volume: 2026-03-09

Abstract: Intraocular pressure is tightly regulated by the conventional outflow tissues, preventing ocular hypertension that leads to neurodegeneration of the optic nerve, or glaucoma. Although macrophages reside throughout the conventional outflow tract, their role in regulating intraocular pressure remains unknown. Using macrophage lineage-tracing approaches, we uncovered a dual macrophage ontogeny with distinct spatial organization across the mouse lifespan. Long-lived resident tissue macrophages were concentrated in the trabecular meshwork and Schlemm’s canal, whereas steady-state monocyte-derived macrophages were abundant around distal vessels. Specific depletion of resident tissue macrophages triggered increased intraocular pressure and outflow resistance, linked to aberrant extracellular matrix turnover in the resistance-generating tissues of the trabecular meshwork. In contrast, dysregulated physiology and tissue remodeling were not observed when monocyte-derived macrophages were depleted. Altogether, we show ontogeny- and tissue-specific macrophage functions within the outflow tract, uncovering the integral homeostatic role of resident tissue macrophages in resistance-generating tissues whose dysfunction is responsible for glaucoma.

DOI: 10.1016/j.immuni.2026.01.025

Source: https://www.cell.com/immunity/abstract/S1074-7613(26)00046-4