莫纳什大学Marcus J. Robinson小组宣布他们揭示了长寿IgE浆细胞通过一种navitoclax敏感型生存程序持续存在于次级淋巴组织中。相关论文于2025年11月4日发表于国际顶尖学术期刊《免疫学》杂志上。

该研究团队检查了IgE抗体分泌细胞（ASCs）的寿命，以确定抑制过敏的IgE是来自长寿命细胞的贡献，还是更多地依赖于持续的ASC产生。在单核主题空气过敏中，IgE ASCs局限于肺、纵隔淋巴结、脾脏和骨髓（BM）。停止接触过敏原后，IgE ASC的产生持续数月。该研究团队发现长寿命的IgE ASCs主要存在于BM外，半衰期超过49天；相比之下，大多数IgE ASCs的半衰期为3天。长寿命的IgE ASCs在表型上成熟，变为静止状态，保留其表面B细胞受体，但显示BM归巢受体CXCR4的低表达。它们在等级上更依赖navitoclax敏感的抗凋亡分子BCL2、BCLXL和BCLW，而不是MCL1。它们，短寿命IgE ASCs的持续产生和BM外长寿命IgE ASCs的保留共同驱动IgE的持久性，使过敏性疾病永续存在。

研究人员表示，长期过敏可表现出循环免疫球蛋白E （IgE）的持续浓度。

附：英文原文

Title: Long-lived IgE plasma cells persist in secondary lymphoid tissues using a navitoclax-sensitive survival program

Author: Zhoujie Ding, Mark R. Dowling, Adam K. Wade-Vallance, Alexandra R. Dvorscek, Catherine Pitt, Jesse Mulder, Kristy O’Donnell, Craig McKenzie, Alexandra Bosak Karaviotis, Julia Scrofani, Olaf Perdijk, Danika L. Hill, Isaak Quast, David M. Tarlinton, Christopher D.C. Allen, Marcus J. Robinson

Issue&Volume: 2025-11-04

Abstract: Long-term allergies can exhibit persistent concentrations of circulating immunoglobulin E (IgE). Here, we examined the lifespan of IgE antibody-secreting cells (ASCs) to determine whether the IgE that sustains allergies receives contributions from long-lived cells or relies more heavily on constant ASC production. In mouse aeroallergy, IgE ASCs localized to the lungs, mediastinal lymph nodes, spleen, and bone marrow (BM). IgE ASC production continued for months after allergen exposure ceased. We identified long-lived IgE ASCs residing predominantly outside the BM, with a half-life exceeding 49 days; in contrast, most IgE ASCs had a 3-day half-life. Long-lived IgE ASCs matured phenotypically, became quiescent, retained their surface B cell receptors, but showed low expression of the BM homing receptor CXCR4. They were hierarchically more reliant on the navitoclax-sensitive anti-apoptotic molecules BCL2, BCLXL, and BCLW than MCL1. Thus, continual production of short-lived IgE ASCs and retention of long-lived IgE ASCs outside the BM together drive IgE persistence, perpetuating allergic disease.

DOI: 10.1016/j.immuni.2025.10.006

Source: https://www.cell.com/immunity/abstract/S1074-7613(25)00460-1