Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Hypervirulent <i>M. tuberculosis</i> W/Beijing Strains Upregulate Type I IFNs and Increase Expression of Negative Regulators of the Jak-Stat Pathway

1 Nov 2005

Abstract excerpt

The role of type I interferons (IFNs) in the host response to bacterial infections is controversial. Here, we examined the role of IFN-alpha/beta in the murine response to infection with Mycobacterium tuberculosis, using wildtype mice, mice with impaired signaling through the type I IFN receptor (IFNAR), and mice treated to reduce levels of type I IFNs. In this study, we used virulent clinical isolates of M....

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Cytokine Signaling Pathways and Interactions
Share to interferon and immune responses
Share to Tuberculosis Research and Epidemiology

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 16318583
DOI: 10.1089/jir.2005.25.694

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Hypervirulent <i>M. tuberculosis</i> W/Beijing Strains Upregulate Type I IFNs and Increase Expression of Negative Regulators of the Jak-Stat PathwayPMID 16318583Read ↗

Pathogenicity of Type I Interferons in Mycobacterium tuberculosisSemantic proximity Read ↗

Type I Interferons in the Pathogenesis of Tuberculosis: Molecular Drivers and Immunological ConsequencesSemantic proximity Read ↗

Interleukin-1 receptor antagonist mediates type I interferon-driven susceptibility to <i>Mycobacterium tuberculosis</i>Semantic proximity Read ↗

Noncanonical T cell responses are associated with protection from tuberculosis in mice and humansSemantic proximity Read ↗

Type I IFN signaling in the absence of IRGM1 promotes <i>M. tuberculosis</i> replication in immune cells by suppressing T cell responsesSemantic proximity Read ↗

Inhibition of Type I Interferon Signaling Abrogates Early Mycobacterium bovis InfectionSemantic proximity Read ↗

Genome-Wide Expression Profiling Identifies Type 1 Interferon Response Pathways in Active TuberculosisSemantic proximity Read ↗

Shared and distinct responses of human and murine alveolar macrophages and monocyte-derived macrophages to <i>Mycobacterium tuberculosis</i>Semantic proximity Read ↗

Type I IFN signaling triggers immunopathology in tuberculosis‐susceptible mice by modulating lung phagocyte dynamicsSemantic proximity Read ↗

Early cellular mechanisms of type I interferon-driven susceptibility to tuberculosisSemantic proximity Read ↗

<i>Mycobacterium tuberculosis</i> Triggers Host Type I IFN Signaling To Regulate IL-1β Production in Human MacrophagesSemantic proximity Read ↗

A protective role for type I interferon signaling following infection with Mycobacterium tuberculosis carrying the rifampicin drug resistance-conferring RpoB mutation H445Y.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.