斯坦福大学王浡团队取得一项新突破。他们提出了破裂细胞的爆炸性细胞毒性是激素监测和免疫防御的桥梁。这一研究成果发表在2026年6月2日出版的国际学术期刊《细胞》上。
研究小组在再生涡虫中发现了“破裂母细胞”，这是一种以前未知的细胞毒性腺细胞类型。破裂母细胞经历爆炸性细胞死亡，“破裂”，由激活素触发，激活素是一种作为炎症细胞因子的多功能激素。通过蛋白质注射、基因嵌合或细菌感染引起的过量激活素引发细胞破裂，释放出强效的可分化细胞毒性物质，能够在几分钟内消除附近的细胞、细菌甚至哺乳动物细胞。破裂母细胞消融术抑制炎症，但损害细菌清除，突出其广谱免疫功能。在机制上不同于已知的细胞毒性和细胞死亡机制，破裂的爆炸性依赖于内质网（ER）来源的钙和细胞骨架依赖的信号放大。破裂细胞样细胞在不同的基侧动物中似乎是保守的，这意味着一个古老的进化起源。这些发现揭示了一种将激素调节与免疫防御相结合的策略，并扩大了进化免疫创新的领域。
据悉，目前对细胞毒性免疫的理解是由造血来源的细胞——T细胞、自然杀伤细胞和中性粒细胞形成的。
附：英文原文
Title: Explosive cytotoxicity of ruptoblasts bridges hormone surveillance and immune defense
Author: Chew Chai, Eliya Sultan, Souradeep R. Sarkar, Lihan Zhong, Dania Nanes Sarfati, Orly Gershoni-Yahalom, Christine Jacobs-Wagner, Hawa Racine Thiam, Benyamin Rosental, Bo Wang
Issue&Volume: 2026-06-02
Abstract: Current understanding of cytotoxic immunity is shaped by hematopoietic-derived cells—T cells, natural killer cells, and neutrophils. Here, we identify “ruptoblasts,” a previously unknown cytotoxic glandular cell type in regenerative planarian flatworms. Ruptoblasts undergo an explosive cell death, “ruptosis,” triggered by activin, a multifunctional hormone acting as an inflammatory cytokine. Excessive activin—induced through protein injection, genetic chimerism, or bacterial infection—initiates ruptosis, discharging potent diffusible cytotoxic agents capable of eliminating nearby cells, bacteria, and even mammalian cells within minutes. Ruptoblast ablation suppresses inflammation but compromises bacterial clearance, highlighting their broad-spectrum immune functions. Mechanistically distinct from known cytotoxic and cell death mechanisms, the explosive nature of ruptosis relies on endoplasmic reticulum (ER)-derived calcium and cytoskeleton-dependent signal amplification. Ruptoblast-like cells appear conserved in diverse basal bilaterians, implying an ancient evolutionary origin. These findings unveil a strategy coupling hormonal regulation with immune defense and expand the landscape of evolutionary immune innovations.
DOI: 10.1016/j.cell.2026.05.008
Source: https://www.cell.com/cell/abstract/S0092-8674(26)00567-2