ArticlePloS one2009
TLR2-dependent inhibition of macrophage responses to IFN-gamma is mediated by distinct, gene-specific mechanisms.
Article in PloS one, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 27 citations in OpenAlex.
- Article
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- Metformin, Empagliflozin, and Their Combination Modulate Ex-Vivo Macrophage Inflammatory Gene Expression.International journal of molecular sciences · 2023Article
- Gut microbiome-derived glycine lipids are diet-dependent modulators of hepatic injury and atherosclerosis.Journal of lipid research · 2022Article
- Mitochondrial respiration contributes to the interferon gamma response in antigen-presenting cells.eLife · 2021Article
- DGCR8 deficiency impairs macrophage growth and unleashes the interferon response to mycobacteria.Life science alliance · 2021Article
- STAT1 is a sex-specific tumor suppressor in colitis-associated colorectal cancer.Molecular oncology · 2018Article
- B Cells Producing Type I IFN Modulate Macrophage Polarization in Tuberculosis.American journal of respiratory and critical care medicine · 2018Article
- Regulation of the maturation of human monocytes into immunosuppressive macrophages.Blood advances · 2017Article
- Immunotherapy for tuberculosis: future prospects.ImmunoTargets and therapy · 2016Review
- Redefining the transcriptional regulatory dynamics of classically and alternatively activated macrophages by deepCAGE transcriptomics.Nucleic acids research · 2015Article
- Evidence for postinitiation regulation of mRNA biogenesis in tuberculosis.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Mouse forestomach carcinoma cells immunosuppress macrophages through transforming growth factor-β1.Molecular medicine reports · 2012Article
- Chemokine CXCL11 links microbial stimuli to intestinal inflammation.Clinical and experimental immunology · 2011Article
- Transmission of endoplasmic reticulum stress and pro-inflammation from tumor cells to myeloid cells.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Review
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Mycobacterium tuberculosis uses multiple mechanisms to avoid elimination by the immune system. We have previously shown that M. tuberculosis can inhibit selected macrophage responses to IFN-gamma through TLR2-dependent and -independent mechanisms. To specifically address the role of TLR2 signaling in mediating this inhibition, we stimulated macrophages with the specific TLR2/1 ligand Pam(3)CSK(4) and assayed responses to IFN-gamma. Pam(3)CSK(4) stimulation prior to IFN-gamma inhibited transcription of the unrelated IFN-gamma-inducible genes, CIITA and CXCL11. Surface expression of MHC class II and secretion of CXCL11 were greatly reduced as well, indicating that the reduction in transcripts had downstream effects. Inhibition of both genes required new protein synthesis. Using chromatin immunoprecipitation, we found that TLR2 stimulation inhibited IFN-gamma-induced RNA polymerase II binding to the CIITA and CXCL11 promoters. Furthermore, TATA binding protein was unable to bind the TATA box of the CXCL11 promoter, suggesting that assembly of transcriptional machinery was disrupted. However, TLR2 stimulation affected chromatin modifications differently at each of the inhibited promoters. Histone H3 and H4 acetylation was reduced at the CIITA promoter but unaffected at the CXCL11 promoter. In addition, NF-kappaB signaling was required for inhibition of CXCL11 transcription, but not for inhibition of CIITA. Taken together, these results indicate that TLR2-dependent inhibition of IFN-gamma-induced gene expression is mediated by distinct, gene-specific mechanisms that disrupt binding of the transcriptional machinery to the promoters.
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