Evidence map›Paper›PMID 41896204›Full record

ArticleCell death discovery2026

Variant-divergent death: Omicron intensifies bystander T-cell apoptosis via GDF15-BCL2L13.

Chao Gao, Hanbing Chen, Ying Chi, Xinxing Lu, Jiahuang Li, Ying Tang, Ruixuan Yu, Nan Shi, Ling Liu, Jianfeng Xie and 3 more

Abstract read
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In one paragraph

Article in Cell death discovery, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors.

Chao Gao *Jiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.
Hanbing Chen *Jiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.
Ying Chi *Jiangsu Provincial Center for Disease Control and Prevention, NHC Key laboratory of Enteric Pathogenic Microbiology, Nanjing, China.
Xinxing LuDepartment of Critical Care Medicine, Taizhou School of Clinical Medicine, The Affiliated Taizhou People's Hospital of Nanjing Medical University, Taizhou, China.
Jiahuang LiSchool of Biopharmacy, China Pharmaceutical University, Nanjing, China.
Ying TangJiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.ORCID http://orcid.org/0000-0002-9526-9613
Ruixuan YuJiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.
Nan ShiJiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.
Ling LiuJiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.
Jianfeng XieJiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China.ORCID http://orcid.org/0000-0002-6097-9172
Haibo QiuJiangsu Provincial Key Laboratory of Critical Care Medicine, Department of Critical Care Medicine, Zhongda Hospital, School of Medicine, Southeast University, Nanjing, China. haiboq2000@163.com.
Jie ChaoDepartment of Physiology, School of Medicine, Southeast University, Nanjing, China. chaojie@seu.edu.cn.ORCID http://orcid.org/0000-0002-7800-3557
Shufeng LiDepartment of Biochemistry, School of Medicine, Southeast University, Nanjing, China. shufengli@seu.edu.cn.ORCID http://orcid.org/0000-0003-4857-4532

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSevere Omicron cases present profound lymphocytopenia, suggesting variant-specific immune injury.

resultsWe identify CD63 as a conserved T-cell host factor supporting ACE2-independent SARS-CoV-2 entry. Despite lower intracellular viral loads than the ancestral strain, Omicron elicits enhanced T-cell apoptosis largely through a bystander mechanism. Omicron-stimulated epithelial cells secrete GDF15, which upregulates the pro-apoptotic protein BCL2L13 in T cells and thereby remotely accelerates apoptosis in uninfected bystanders. Functionally, recombinant GDF15 increases BCL2L13 and apoptosis, while genetic dampening of BCL2L13 blunts Omicron-specific high-intensity bystander death. In clinical samples, plasma GDF15 associates with mortality, SOFA scores, and lower lymphocyte counts, bridging the epithelial-immune axis to patient outcomes.

conclusionsOur data delineate a two-track model of Omicron immune injury-CD63-enabled T-cell entry plus GDF15-BCL2L13-driven bystander apoptosis-that reconciles lower epithelial cytopathicity with deeper T-cell depletion in critical disease. These findings nominate the GDF15-BCL2L13 axis as a mechanistic marker and potential point of intervention.

Identifiers

PMID41896204
PMCPMC13150034

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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.