ArticleJournal of immunology (Baltimore, Md. : 1950)2012
ITAM-coupled receptors inhibit IFNAR signaling and alter macrophage responses to TLR4 and Listeria monocytogenes.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. 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, 25 citations in OpenAlex.
- Modulation of TNF-induced macrophage polarization by synovial fibroblasts.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Targeting LAMP2 synergizes with gemcitabine to inhibit bladder cancer progression via modulating STING degradation and regulating macrophage phenotypes.Apoptosis : an international journal on programmed cell death · 2026Article
- CD11b suppresses TLR activation of nonclassical monocytes to reduce primary graft dysfunction after lung transplantation.The Journal of clinical investigation · 2022Article
- Type I Interferon-Mediated Regulation of Antiviral Capabilities of Neutrophils.International journal of molecular sciences · 2021Review
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- CD11b activation suppresses TLR-dependent inflammation and autoimmunity in systemic lupus erythematosus.The Journal of clinical investigation · 2017Article
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- Fungal pattern receptors down-regulate the inflammatory response by a cross-inhibitory mechanism independent of interleukin-10 production.Immunology · 2017Article
- Cross Talk between Inhibitory Immunoreceptor Tyrosine-Based Activation Motif-Signaling and Toll-Like Receptor Pathways in Macrophages and Dendritic Cells.Frontiers in immunology · 2017Review
- FcεRI γ-Chain Negatively Modulates Dectin-1 Responses in Dendritic Cells.Frontiers in immunology · 2017Article
- Opposing regulation of the late phase TNF response by mTORC1-IL-10 signaling and hypoxia in human macrophages.Scientific reports · 2016Article
- Complement receptor 3 mediates renal protection in experimental C3 glomerulopathy.Kidney international · 2016Article
- Rare variants at 16p11.2 are associated with common variable immunodeficiency.The Journal of allergy and clinical immunology · 2015Article
- Regulation of type I interferon responses.Nature reviews. Immunology · 2014Review
- Phagocytosis is the main CR3-mediated function affected by the lupus-associated variant of CD11b in human myeloid cells.PloS one · 2013Article
- Loss of DAP12 and FcRγ drives exaggerated IL-12 production and CD8(+) T cell response by CCR2(+) Mo-DCs.PloS one · 2013Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
ITAM-coupled receptors play an essential role in regulating macrophage activation and function by cross-regulating signaling from heterologous receptors. We investigated mechanisms by which ITAM-associated receptors inhibit type I IFN (IFN-α/β) signaling in primary human macrophages and tested the effects of simultaneous ligation of ITAM-associated receptors and TLR4 on TLR4-induced Jak-STAT signaling that is mediated by autocrine IFN-β. Preligation of ITAM-coupled β2 integrins and FcγRs inhibited proximal signaling by the type I IFN receptor IFNAR. Cross-inhibition of IFNAR signaling by β2 integrins resulted in decreased Jak1 activation and was mediated by partial downregulation of the IFNAR1 subunit and MAPK-dependent induction of USP18, which blocks the association of Jak1 with IFNAR2. Simultaneous engagement of ITAM-coupled β2 integrins or Dectin-1 with TLR4 did not affect TLR4-induced direct activation of inflammatory target genes such as TNF or IL6 but abrogated subsequent induction of IFN response genes that is mediated by autocrine IFN-β signaling. Type I IFNs promote macrophage death postinfection by Listeria monocytogenes. Consequently, attenuation of IFN responses by β2 integrins protected primary human macrophages from L. monocytogenes-induced apoptosis. These results provide a mechanism for cross-inhibition of type I IFN signaling by ITAM-coupled β2 integrins and demonstrate that ITAM signaling qualitatively modulates macrophage responses to pathogen-associated molecular patterns and pathogens by selectively suppressing IFN responses.
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