Article in Science immunology, 2026. 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.
Journal of medical microbiology · 2026
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.
Shota TorigoeLaboratory of Molecular Immunology, Immunology Frontier Research Center, Osaka University, Osaka, Japan.ORCID 0000-0002-4884-3686
Sumayah SalieCMM AFRICA Medical Mycology Research Unit, Institute of Infectious Diseases and Molecular Medicine (IDM), University of Cape Town, Cape Town 7925, South Africa.ORCID 0000-0002-3608-8820
Roanne KeetonCMM AFRICA Medical Mycology Research Unit, Institute of Infectious Diseases and Molecular Medicine (IDM), University of Cape Town, Cape Town 7925, South Africa.ORCID 0000-0003-4808-9756
Beren AylanHost-Pathogen Interactions in Tuberculosis Laboratory, Francis Crick Institute, London, UK.ORCID 0009-0008-7741-2712
Ben J AppelmelkMedical Microbiology and Infection Control, Amsterdam University Medical Centers, Amsterdam, Netherlands.ORCID 0000-0002-4274-5911
David L WilliamsDepartment of Surgery, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA.ORCID 0000-0002-4586-9290
Douglas W LowmanDepartment of Surgery, James H. Quillen College of Medicine, East Tennessee State University, Johnson City, TN, USA.ORCID 0000-0002-2080-3447
Toshihiko SugikiLaboratory of Molecular Biophysics, Institute for Protein Research, Osaka University, Osaka, Japan.ORCID 0000-0003-1716-1241
Sohkichi MatsumotoDepartment of Bacteriology, Graduate School of Medical and Dental Science, Niigata University, Niigata, Japan.
Akira KawanoDepartment of Microbiology and Molecular Genetics, Mie University Graduate School of Medicine, Mie, Japan.ORCID 0009-0003-9470-6388
Satoru MizunoInstitute for Vaccine Research and Development, Hokkaido University, Hokkaido, Japan.ORCID 0009-0001-9564-9755
Kazuhiro MatsuoInstitute for Vaccine Research and Development, Hokkaido University, Hokkaido, Japan.ORCID 0000-0002-2329-887X
Jonas N SøndergaardHuman Single Cell Immunology Team, Center for Infectious Disease Education and Research (CiDER), Osaka University, Osaka, Japan.ORCID 0000-0002-4438-6756
James B WingHuman Single Cell Immunology Team, Center for Infectious Disease Education and Research (CiDER), Osaka University, Osaka, Japan.ORCID 0000-0002-3462-1003
Maxine A HöftCMM AFRICA Medical Mycology Research Unit, Institute of Infectious Diseases and Molecular Medicine (IDM), University of Cape Town, Cape Town 7925, South Africa.ORCID 0000-0002-5719-9458
Romey ShoesmithMedical Research Council Centre for Medical Mycology, University of Exeter, Exeter, UK.ORCID 0000-0001-6629-6172
Mthawelanga NdenganeCentre for Infectious Diseases Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town, South Africa.
Anna K CoussensCentre for Infectious Diseases Research in Africa, Institute of Infectious Disease and Molecular Medicine, University of Cape Town, Cape Town, South Africa.ORCID 0000-0002-7086-2621
Janet A WillmentMedical Research Council Centre for Medical Mycology, University of Exeter, Exeter, UK.ORCID 0000-0002-7040-0857
Maximiliano G GutierrezHost-Pathogen Interactions in Tuberculosis Laboratory, Francis Crick Institute, London, UK.ORCID 0000-0003-3199-0337
Jennifer Claire HovingCMM AFRICA Medical Mycology Research Unit, Institute of Infectious Diseases and Molecular Medicine (IDM), University of Cape Town, Cape Town 7925, South Africa.
Sho YamasakiDepartment of Molecular Immunology, Research Institute for Microbial Diseases, Osaka University, Osaka, Japan.ORCID 0000-0002-5184-6917
Gordon D BrownCMM AFRICA Medical Mycology Research Unit, Institute of Infectious Diseases and Molecular Medicine (IDM), University of Cape Town, Cape Town 7925, South Africa.ORCID 0000-0002-0287-5383
Funding
Medical Research Council CC2081Medical Research Council MR/N006364/1Medical Research Council MR/N006364/2Wellcome Trust 102705Wellcome Trust 203135Wellcome Trust 209293Wellcome Trust 217163Wellcome Trust CC2081
6 · The paper itself
Abstract
Mycobacteria have a cell envelope that can act as a shield against host defense. This study shows that mycobacteria survive in host macrophages by targeting the innate host receptor dectin-1 through a noncanonical ligand. Compared with wild-type (WT) mice, dectin-1-deficient mice were more resistant to infection to mycobacteria. Dectin-1-deficient mice presented with substantially reduced bacterial burdens, inflammatory cytokines, and infiltrating myeloid cells, such as neutrophils and macrophages. Intracellular survival of these bacteria was reduced in macrophages derived from dectin-1-deficient mice compared with those from WT mice. Cellular characterization of mycobacteria-infected macrophages indicated that the presence of dectin-1 altered phagosomal maturation and association with markers of autophagy. Activity-based purification and nuclear magnetic resonance spectrometry identified branched α-glucan as the dectin-1 mycobacterial ligand. This branched glucan was essential for activating dectin-1. These results show that mycobacterial α-glucan targets dectin-1 to facilitate intracellular bacterial survival.
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.
Mycobacterial α-glucans hijack dectin-1 to facilitate intracellular bacterial survival. · full record | OpenQuestion