Cited by 601Tuberculosis Research and EpidemiologyImmune Response and InflammationImmune responses and vaccinations

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TLR9 regulates Th1 responses and cooperates with TLR2 in mediating optimal resistance to Mycobacterium tuberculosis

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Bafica, Andre, Scanga, Charles A., Feng, Carl G., Leifer, Cynthia, Cheever, Allen, Sher, Alan·2005·The Journal of Experimental Medicine

DOI 10.1084/jem.20051782PMC PMC2212963

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Abstract

To investigate the role of Toll-like receptor (TLR)9 in the immune response to mycobacteria as well as its cooperation with TLR2, a receptor known to be triggered by several major mycobacterial ligands, we analyzed the resistance of TLR9(-/-) as well as TLR2/9 double knockout mice to aerosol infection with Mycobacterium tuberculosis. Infected TLR9(-/-) but not TLR2(-/-) mice displayed defective mycobacteria-induced interleukin (IL)-12p40 and interferon (IFN)-gamma responses in vivo, but in common with TLR2(-/-) animals, the TLR9(-/-) mice exhibited only minor reductions in acute resistance to low dose pathogen challenge. When compared with either of the single TLR-deficient animals, TLR2/9(-/-) mice displayed markedly enhanced susceptibility to infection in association with combined defects in proinflammatory cytokine production in vitro, IFN-gamma recall responses ex vivo, and altered pulmonary pathology. Cooperation between TLR9 and TLR2 was also evident at the level of the in vitro response to live M. tuberculosis, where dendritic cells and macrophages from TLR2/9(-/-) mice exhibited a greater defect in IL-12 response than the equivalent cell populations from single TLR9-deficient animals. These findings reveal a previously unappreciated role for TLR9 in the host response to M. tuberculosis and illustrate TLR collaboration in host resistance to a major human pathogen.

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A Toll-like receptor recognizes bacterial DNA
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Authors: Bafica, A., Scanga, C. A., Feng, C. G., Leifer, C., Cheever, A., & Sher, A.
Affiliations: 1Immunobiology Section, Laboratory of Parasitic Diseases
National Institute of Allergy and Infectious Diseases (US)
National Institutes of Health (US)
Biomedical Research Institute (US)
ORCID: Scanga, Charles A.
Feng, Carl G.
Leifer, Cynthia
Sher, Alan
Venue: The Journal of Experimental Medicine
Publisher: Rockefeller University Press
Published: 2005-12-19
Volume: 202
Issue: 12
Pages: 1715-1724
ISSN: 0022-1007 (ISSN-L)
1540-9538
DOI: 10.1084/jem.20051782
PMC: PMC2212963
OpenAlex: W2159112596
Cited by: 601
References: 64
Citations by year: 2026: 5 · 2025: 12 · 2024: 11 · 2023: 16 · 2022: 18 · 2021: 26 · 2020: 17 · 2019: 28 · 2018: 29 · 2017: 25 · 2016: 37 · 2015: 27 · 2014: 35 · 2013: 29 · 2012: 48
FWCI: 23.88
Type: journal article
Language: en
Open access: green
europepmc.org
Licence: cc-by-nc-sa
Locations: The Journal of Experimental Medicine (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion, cc-by-nc-sa)
PubMed Central (publishedVersion, cc-by-nc-sa)
PubMed (publishedVersion)
Topics: Health Sciences › Medicine › Infectious Diseases › Tuberculosis Research and Epidemiology
Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
Life Sciences › Immunology and Microbiology › Immunology › Immune responses and vaccinations
Keywords: TLR9, TLR2, Mycobacterium tuberculosis, Th1 response, IL-12p40, interferon-gamma, aerosol infection, dendritic cells, macrophages, inflammatory cytokines, lung pathology
MeSH terms: Animals, Antigen-Presenting Cells, Flow Cytometry, Immunity, Innate, Lung, Mycobacterium tuberculosis, Tuberculosis, Cytokines, DNA Primers, Mice, Knockout, Th1 Cells, Reverse Transcriptase Polymerase Chain Reaction, Toll-Like Receptor 9, Mice

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TLR9 regulates Th1 responses and cooperates with TLR2 in mediating optimal resistance to Mycobacterium tuberculosis

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