ArticlePloS one2014
Fc gamma receptor IIb on GM-CSF macrophages controls immune complex mediated inhibition of inflammatory signals.
Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 18 citations in OpenAlex.
- IgA2 ACPA Drives a Hyper-Inflammatory Phenotype in Macrophages via ATP Synthase and COX2.European journal of immunology · 2025Article
- Defining genetic diversity of rhesus macaque Fcγ receptors with long-read RNA sequencing.Frontiers in immunology · 2023Article
- Review of the Potential Therapeutic Effects and Molecular Mechanisms of Resveratrol on Endometriosis.International journal of women's health · 2023Review
- Promising targets and drugs in rheumatoid arthritis: a module-based and cumulatively scoring approach.Bone & joint research · 2020Article
- Association Between ApoA-I (Apolipoprotein A-I) Immune Complexes and Adverse Cardiovascular Events-Brief Report.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- An Engineered Human Fc variant With Exquisite Selectivity for FcγRIIIaFrontiers in immunology · 2019Article
- Role of NS1 antibodies in the pathogenesis of acute secondary dengue infection.Nature communications · 2018Article
- Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundIn rheumatoid arthritis (RA) macrophages play a major role in amplifying synovial inflammation. Important activating signals are those induced by Toll-like receptor (TLR) ligands and by activated T cells. The balance between activating and inhibitory Fc gamma receptors (FcγRs) on macrophages might be crucial in modulating these inflammatory responses. The purpose of this study was to determine FcγR expression on pro- and anti-inflammatory macrophages (gmMφ and mMφ, respectively) and identify functional consequences on immune complex uptake and macrophage activation.
methodsHuman monocytes were isolated and differentiated into gmMφ and mMφ. A full FcγR characterization of both macrophage subtypes was performed and uptake of fluorescent immune complexes (ICs) was determined. FcγRIIb isoforms were determined by qPCR. Macrophages were stimulated via different TLRs or cytokine activated T cells in the presence or absence of ICs and cytokine production was determined. Blocking studies were performed to look into the pathways involved.
resultsmMφ expressed high levels of the activating FcγRIIa and FcγRIII and low levels of the inhibitory FcγRIIb, while the FcγR balance on gmMφ was shifted towards the inhibitory FcγRIIb. This was accompanied by a clear increase in FcγRIIb1 mRNA expression in gmMφ. This resulted in higher IC uptake by mMφ compared to gmMφ. Furthermore, FcγR-mediated stimulation of gmMφ inhibited TLR2, 3, 4 and 7/8 mediated cytokine production via FcγRIIb and PI3K signaling. In addition, gmMφ but not mMφ produced TNFα upon co-culture with cytokine activated T cells, which was reduced by IC binding to FcγRIIb. The latter was dependent on PI3K signaling and COX2.
conclusionsFcγR expression patterns on gmMφ and mMφ are significantly different, which translates in clear functional differences further substantiating FcγRIIb as an interesting target for inflammation control in RA and other autoimmune/inflammatory diseases.
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