Evidence map›Paper›PMID 42229422›Full record

ArticleCell2026

Explosive cytotoxicity of ruptoblasts bridges hormone surveillance and immune defense.

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

Abstract read
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In one paragraph

Article in Cell, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors.

Chew ChaiDepartment of Bioengineering, Stanford University, Stanford, CA 94305, USA.
Eliya SultanShraga Segal Department of Microbiology, Immunology, and Genetics, Faculty of Health Sciences, Center for Regenerative Medicine and Stem Cells, Ben Gurion University of the Negev, Be'er Sheva 8410501, Israel.
Souradeep R SarkarDepartment of Bioengineering, Stanford University, Stanford, CA 94305, USA.
Lihan ZhongDepartment of Bioengineering, Stanford University, Stanford, CA 94305, USA.
Dania Nanes SarfatiDepartment of Biology, Stanford University, Stanford, CA 94305, USA.
Orly Gershoni-YahalomShraga Segal Department of Microbiology, Immunology, and Genetics, Faculty of Health Sciences, Center for Regenerative Medicine and Stem Cells, Ben Gurion University of the Negev, Be'er Sheva 8410501, Israel.
Christine Jacobs-WagnerDepartment of Biology, Stanford University, Stanford, CA 94305, USA; Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA; Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA; Sarafan ChEM-H, Stanford University, Stanford, CA 94305, USA.
Hawa Racine ThiamDepartment of Bioengineering, Stanford University, Stanford, CA 94305, USA; Department of Microbiology and Immunology, Stanford University School of Medicine, Stanford, CA 94305, USA; Sarafan ChEM-H, Stanford University, Stanford, CA 94305, USA.
Benyamin RosentalShraga Segal Department of Microbiology, Immunology, and Genetics, Faculty of Health Sciences, Center for Regenerative Medicine and Stem Cells, Ben Gurion University of the Negev, Be'er Sheva 8410501, Israel. Electronic address: rosentab@post.bgu.ac.il.
Bo WangDepartment of Bioengineering, Stanford University, Stanford, CA 94305, USA; Department of Developmental Biology, Stanford University School of Medicine, Stanford, CA 94305, USA. Electronic address: wangbo@stanford.edu.

Funding

Comparative systems biology defines regulatory mechanisms in whole-body regenerationR35GM138061 · NIGMS · STANFORD UNIVERSITY · PI Bo Wang · 2020 to 2026
$2.5M
NIGMS NIH HHS R35 GM138061
6 · The paper itself

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.

Indexed as

PlanariansActivinsAnimalsCell DeathActivinsactivin signalingcell death/destructioncytotoxicityevolution of immune systemextreme cell biologygenetic chimerasglandular/secretory cell typeshormonal surveillanceplanarian

Identifiers

PMID42229422

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.