Evidence map›Paper›PMID 41030999›Full record

ArticlebioRxiv : the preprint server for biology2025

Tissue-wide profiling of human lungs reveals spatial sequestration of macrophages in tuberculosis.

Wei Xiao, Andrew J Sawyer, Siwei Mo, Xinyu Bai, Qinzhu Yang, Yi Gao, Timothy Fielder, Yue Zhang, Youchao Dai, Qianting Yang and 13 more

Abstract readPreprint
PubMed Full text at PMC Publisher
In one paragraph

Article in bioRxiv : the preprint server for biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. Article
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

23 authors.

Wei XiaoSchool of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.
Andrew J SawyerSchool of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.
Siwei MoGuangdong Key Laboratory of Infection Immunity and Inflammation, Department of Pathogen Biology, Shenzhen University School of Medicine, Shenzhen, China.
Xinyu BaiSchool of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.
Qinzhu YangSchool of Biomedical Engineering, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.
Yi GaoSchool of Biomedical Engineering, Shenzhen University Medical School, Shenzhen University, Shenzhen, China.
Timothy FielderDepartment of Tissue Pathology and Diagnostic Oncology, Royal Prince Alfred Hospital, Camperdown, Australia.
Yue ZhangGuangdong Key Laboratory of Infection Immunity and Inflammation, Department of Pathogen Biology, Shenzhen University School of Medicine, Shenzhen, China.
Youchao DaiGuangdong Key Laboratory of Infection Immunity and Inflammation, Department of Pathogen Biology, Shenzhen University School of Medicine, Shenzhen, China.
Qianting YangGuangdong Key Lab for Diagnosis and Treatment of Emerging Infectious Diseases, Shenzhen Third People's Hospital, Shenzhen, China.
Yi CaiGuangdong Key Laboratory of Infection Immunity and Inflammation, Department of Pathogen Biology, Shenzhen University School of Medicine, Shenzhen, China.ORCID 0000-0002-1363-2328
Guanggui DingDepartment of Thoracic Surgery, Shenzhen People's Hospital (The Second Clinical Medical College, Jinan University; The First Affiliated Hospital, Southern University of Science and Technology), Shenzhen, China.
Guofang DengGuangdong Key Lab for Diagnosis and Treatment of Emerging Infectious Diseases, Shenzhen Third People's Hospital, Shenzhen, China.
Liang FuGuangdong Key Lab for Diagnosis and Treatment of Emerging Infectious Diseases, Shenzhen Third People's Hospital, Shenzhen, China.ORCID 0000-0003-1112-8010
Camelia QuekSchool of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.
James WilmottSchool of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.
Umaimainthan PalendiraSchool of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.
Warwick J BrittonCentenary Institute, The University of Sydney, Sydney, Australia.
Daniel L BarberLaboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Joel D ErnstDivision of Experimental Medicine, Department of Medicine, University of California San Francisco, San Francisco, CA, USA.
Ellis PatrickSchool of Mathematics and Statistics, Faculty of Science, The University of Sydney, Sydney, Australia.ORCID 0000-0002-5253-4747
Carl G FengSchool of Medical Sciences, Faculty of Medicine and Health, The University of Sydney, Sydney, Australia.
Xinchun ChenGuangdong Key Laboratory of Infection Immunity and Inflammation, Department of Pathogen Biology, Shenzhen University School of Medicine, Shenzhen, China.

Funding

Functional dynamics of TB granuloma architecture - Diversity Supplement for Kelley J. MartinezU01AI166309 · NIAID · UNIVERSITY OF CALIFORNIA, SAN FRANCISCO · PI Joel D. Ernst · 2022 to 2026
$3.2M
NIAID NIH HHS U01 AI166309
6 · The paper itself

Abstract

The immune response to human tuberculosis (TB), particularly in the context of complex lung pathology, remains incompletely understood. Here, we employed whole-slide spatial proteomics to map immune cell organization in TB-affected human lung tissues. Our analysis revealed pronounced spatial segregation of major immune cell populations in non-necrotizing TB lesions. At the tissue level, macrophages and lymphocytes formed distinct cellular communities associated with specific pathological features. At the lesion level, macrophages and B cells showed an inverse relationship in both abundance and spatial distribution. Proinflammatory T cells preferentially accumulated in macrophage-rich lesions but remained largely separated from macrophages. Interestingly, lesions exhibiting clear segregation between T cells and macrophages were more common in subclinical TB than in active disease. These findings suggest that spatial isolation of macrophages from effector lymphocytes may help temper inflammation and potentially prevent lesion progression to necrosis, while also enabling immune evasion by

Indexed as

humanlung immunityspatial biologytertiary lymphoid structuretissue pathologyTuberculosis

Identifiers

PMID41030999
PMCPMC12478358

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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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.