ArticleThe Journal of biological chemistry2011
Silencing suppressor of cytokine signaling-1 (SOCS1) in macrophages improves Mycobacterium tuberculosis control in an interferon-gamma (IFN-gamma)-dependent manner.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 1 of them a synthesis that pooled it.
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Who cites it
31 citing papers in PubMed, 1 synthesis or guideline pooled it, 59 citations in OpenAlex.
- A meta-analysis of Th1 and Th2 cytokine profiles differentiating tuberculous from malignant pleural effusion.Scientific reports · 2022Pooled it
- Pharmacological inhibition of USP18 improves antibacterial responses and the intracellular control ofFrontiers in immunology · 2026Article
- Immunoregulatory Microenvironment in the Elderly Skin.JID innovations : skin science from molecules to population health · 2025Article
- S-nitrosylation-triggered secretion of mycobacterial PknG leads to phosphorylation of SODD to prevent apoptosis of infected macrophages.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Interactions between CNS and immune cells in tuberculous meningitis.Frontiers in immunology · 2024Review
- Decoding the intricacies: a comprehensive analysis of microRNAs in the pathogenesis, diagnosis, prognosis and therapeutic strategies for COVID-19.Frontiers in medicine · 2024Review
- Article
- HIF-1 stabilization in T cells hampers the control of Mycobacterium tuberculosis infection.Nature communications · 2022Article
- Recombinant BCG to Enhance Its Immunomodulatory Activities.Vaccines · 2022Review
- Role of T cells during the cerebral infection with Trypanosoma brucei.PLoS neglected tropical diseases · 2021Article
- SOCS3 Expression by Thymic Stromal Cells Is Required for Normal T Cell Development.Frontiers in immunology · 2021Article
- H. pylori modulates DC functions via T4SS/TNFα/p38-dependent SOCS3 expression.Cell communication and signaling : CCS · 2020Article
- Suppressors of Cytokine Signaling (SOCS)1 and SOCS3 Proteins Are Mediators of Interleukin-10 Modulation of Inflammatory Responses Induced byMediators of inflammation · 2020Article
- Mycobacteria-Specific T Cells Are Generated in the Lung During Mucosal BCG Immunization or Infection WithFrontiers in immunology · 2020Article
- Primary Role of Suppressor of Cytokine Signaling 1 in Mycobacterium bovis BCG Infection.Infection and immunity · 2018Article
- Temporal changes in macrophage phenotype after peripheral nerve injury.Journal of neuroinflammation · 2018Article
- STAT3 expression by myeloid cells is detrimental for the T- cell-mediated control of infection with Mycobacterium tuberculosis.PLoS pathogens · 2018Article
- Concordant and discordant gene expression patterns in mouse strains identify best-fit animal model for human tuberculosis.Scientific reports · 2017Article
- SOCS1 is a negative regulator of metabolic reprogramming during sepsis.JCI insight · 2017Article
- Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Protection against infection with Mycobacterium tuberculosis demands IFN-γ. SOCS1 has been shown to inhibit responses to IFN-γ and might thereby play a central role in the outcome of infection. We found that M. tuberculosis is a highly efficient stimulator of SOCS1 expression in murine and human macrophages and in tissues from infected mice. Surprisingly, SOCS1 reduced responses to IL-12, resulting in an impaired IFN-γ secretion by macrophages that in turn accounted for a deteriorated intracellular mycobacterial control. Despite SOCS1 expression, mycobacteria-infected macrophages responded to exogenously added IFN-γ. SOCS1 attenuated the expression of the majority of genes modulated by M. tuberculosis infection of macrophages. Using a conditional knockdown strategy in mice, we found that SOCS1 expression by macrophages hampered M. tuberculosis clearance early after infection in vivo in an IFN-γ-dependent manner. On the other hand, at later time points, SOCS1 expression by non-macrophage cells protected the host from infection-induced detrimental inflammation.
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Registered trials
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.