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Cited by 685Tuberculosis Research and EpidemiologyImmune responses and vaccinationsImmune Response and Inflammation

The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.

Immune Control of Tuberculosis by IFN-γ-Inducible LRG-47

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MacMicking, John D., Taylor, Gregory A., McKinney, John D.·2003·Science
DOI 10.1126/science.1088063
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Abstract

Interferon-γ (IFN-γ) provides an essential component of immunity to tuberculosis by activating infected host macrophages to directly inhibit the replication of Mycobacterium tuberculosis ( Mtb ). IFN-γ–inducible nitric oxide synthase 2 (NOS2) is considered a principal effector mechanism, although other pathways may also exist. Here, we identify one member of a newly emerging 47-kilodalton (p47) guanosine triphosphatase family, LRG-47, that acts independently of NOS2 to protect against disease. Mice lacking LRG-47 failed to control Mtb replication, unlike those missing the related p47 guanosine triphosphatases IRG-47 or IGTP. Defective bacterial killing in IFN-γ–activated LRG-47 –/– macrophages was associated with impaired maturation of Mtb -containing phagosomes, vesicles that otherwise recruited LRG-47 in wild-type cells. Thus, LRG-47 may serve as a critical vacuolar trafficking component used to dispose of intracellular pathogens like Mtb .

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Crossref · 10.1126/science.1088063

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Research works printed but not linked: 4

  1. J. D. MacMicking et al., Proc. Natl. Acad. Sci. U.S.A.94, 5423 (1997).
  2. O. Olakamni, L. S. Schlesinger, A. Ahmed, B. E. Britigan, J. Biol. Chem. 277, 49727 (2003).
  3. D. J. Hackam et al., J. Exp. Med. 188, 1351 (1998).
  4. We thank J. Belisle for provision of purified Mtb cell-wall components; R. Steinman for F4/80 antibody; H. Shio for electron microscopy; D. McMurray for aerosol chamber instruction; P. Giannakis D. Phelan R. Rice and A. Sousa for experimental assistance; and A. Francesconi A. Muesch C. Nathan and members of the Section of Microbial Pathogenesis (Yale University School of Medicine) for helpful discussions. Supported by a Howard Hughes Medical Institute Fellowship of the Life Science Research Foundation (J.D.M.) Veterans Administration Merit Review Grant (G.A.T.) Ellison Medical Foundation Sequella Global Tuberculosis Foundation Sinsheimer Fund Irma T. Hirschl Trust and NIH RO1 A1051702 (J. D. McKinney).

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Metadata

Authors
MacMicking, J. D., Taylor, G. A., & McKinney, J. D.
Affiliations
Duke University (US)
Corresponding author
MacMicking, John D.
ORCID
Venue
Science
Publisher
American Association for the Advancement of Science (AAAS)
Published
2003-10-24
Volume
302
Issue
5645
Pages
654-659
ISSN
  • 0036-8075 (ISSN-L)
  • 1095-9203
DOI
10.1126/science.1088063
OpenAlex
W1989883893
Cited by
685
References
31
Citations by year
2026: 11 · 2025: 15 · 2024: 16 · 2023: 21 · 2022: 15 · 2021: 27 · 2020: 23 · 2019: 26 · 2018: 27 · 2017: 21 · 2016: 21 · 2015: 34 · 2014: 31 · 2013: 44 · 2012: 44
FWCI
19.81
Type
journal article
Language
en
Open access
Locations
  • Science (publishedVersion)
  • PubMed (publishedVersion)
  • Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion)
  • Infoscience (Ecole Polytechnique Fédérale de Lausanne) (submittedVersion, cc-by-nc-nd)
Funders
U.S. Public Health Service (R01 A1051702)
Topics
  • Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
  • Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Keywords
tuberculosis, interferon-gamma, Mycobacterium tuberculosis, nitric oxide synthase 2, intracellular pathogen clearance, vacuolar trafficking, host immunity
MeSH terms
Animals, Cells, Cultured, Disease Susceptibility, Female, Hydrogen-Ion Concentration, Immunity, Innate, Interferon-gamma, Macrophage Activation, Macrophages, Male, Mice, Inbred C57BL, Mutation, Mycobacterium tuberculosis, Phagosomes, Tuberculosis, Signal Transduction, Macrophages, Alveolar, Nitric Oxide Synthase, GTP-Binding Proteins, Computational Biology, Reverse Transcriptase Polymerase Chain Reaction, Oligonucleotide Array Sequence Analysis, GTP Phosphohydrolases, Mice, Nitric Oxide Synthase Type II

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