Evidence map›Paper›PMID 42034649›Full record

ArticleNature communications2026

IFNγ blockade in Mycobacterium tuberculosis infected macaques alters the granuloma environment but not bacterial control.

Shunsuke Sakai, Sivaranjani Namasivayam, Keith D Kauffman, Eduardo Fukutani, Artur T L Queiroz, Christine E Nelson, Erin F McCaffrey, Ploenchan Chetchotisakd, Jay Buchanan, Alan Sher and 8 more

Abstract read
In one paragraph

Article in Nature communications, 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
–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

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

18 authors.

Shunsuke SakaiT Lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Sivaranjani NamasivayamImmunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0001-9993-1347
Keith D KauffmanT Lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0001-7208-1565
Eduardo FukutaniLaboratório de Pesquisa Clínica e Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador, Brazil.
Artur T L QueirozLaboratório de Pesquisa Clínica e Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador, Brazil.ORCID http://orcid.org/0000-0003-4908-9993
Christine E NelsonT Lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Erin F McCaffreySpatial Immunology Unit, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Ploenchan ChetchotisakdDivision of Infectious Diseases and Tropical Medicine, Srinagarind Hospital, Khon Kaen University, Khon Kaen, Thailand.
Jay BuchananT Lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.
Alan SherImmunobiology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0001-7053-2895
Carl G FengImmunology and Host Defense Group, Faculty of Medicine and Health, The University of Sydney, Sydney, New South Wales, Australia.ORCID http://orcid.org/0000-0003-4301-4640
Joel D ErnstDivision of Experimental Medicine, Department of Medicine, University of California, San Francisco, CA, USA.ORCID http://orcid.org/0000-0001-9951-6207
Steven M HollandImmunopathogenesis Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0003-3207-5464
Katrin D Mayer-BarberInflammation and Innate Immunity Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0002-0311-3233
Bruno B AndradeLaboratório de Pesquisa Clínica e Translacional, Instituto Gonçalo Moniz, Fundação Oswaldo Cruz, Salvador, Brazil.ORCID http://orcid.org/0000-0001-6833-3811
Christa S ZerbeImmunopathogenesis Section, Laboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0003-4219-0503
Laura E ViaTuberculosis Research Section, Laboratory of Clinical Immunology and Microbiology, Division of Intramural Research, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, USA.ORCID http://orcid.org/0000-0001-6074-9521
Daniel L BarberT Lymphocyte Biology Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD, USA. barberd@niaid.nih.gov.ORCID http://orcid.org/0000-0001-7008-7509

Funding

Division of Intramural Research, National Institute of Allergy and Infectious Diseases (Division of Intramural Research of the NIAID) 1ZIAAI001171-14
6 · The paper itself

Abstract

IFNγ is considered the primary mediator of adaptive immunity to Mycobacterium tuberculosis (Mtb) infection. In mice, control of Mtb requires IFNγ. In humans, IFNγ is critical for resistance to infection with non-tuberculous mycobacteria (NTM), but its relative requirement for control of pulmonary tuberculosis (TB) is less clear. Here we block IFNγR1 signaling in macaques at different times following Mtb infection. IFNγ blockade from day 45 to 49 post-infection rapidly reduced

Indexed as

GranulomaInterferon-gammaMycobacterium tuberculosisTuberculosisTuberculosis, PulmonaryAnimalsAutoantibodiesBacterial LoadFemaleHumansInterferon gamma ReceptorLungMacacaMaleMiceNitric Oxide Synthase Type IIAutoantibodiesInterferon-gammaInterferon gamma ReceptorNitric Oxide Synthase Type IIReceptors, Interferon

Identifiers

PMID42034649
PMCPMC13323717

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.