ArticleFrontiers in immunology2018
IVIg and LPS Co-stimulation Induces IL-10 Production by Human Monocytes, Which Is Compromised by an FcγRIIA Disease-Associated Gene Variant.
Article in Frontiers in immunology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 24 citations in OpenAlex.
- ERK1/2 activation in anti-inflammatory effects and underlying signaling mechanisms.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- System-wide immunoregulation by polyvalent IgG: integrating transcriptomic, miRNA, and proteomic landscapes.Journal of translational medicine · 2026Article
- Effect of Tyrosine-Containing Self-Assembling β-Sheet Peptides on Macrophage Polarization and Inflammatory Response.ACS applied materials & interfaces · 2025Article
- Intravenous immunoglobulin ameliorates doxorubicin-induced intestinal mucositis by inhibiting the Syk/PI3K/Akt axis and ferroptosis.Apoptosis : an international journal on programmed cell death · 2025Article
- Article
- A subset of antibodies targeting citrullinated proteins confers protection from rheumatoid arthritis.Nature communications · 2023Article
- Microfluidic system for immune cell activation and inflammatory cytokine profiling: Application to screening of dietary supplements for anti-inflammatory properties.Biomicrofluidics · 2022Article
- The Functional Role of IgA in the IgM/IgA-Enriched Immunoglobulin Preparation Trimodulin.Biomedicines · 2021Article
- Intravenous immunoglobulin as an important adjunct in the prevention and therapy of coronavirus 2019 disease.Scandinavian journal of immunology · 2021Review
- A monocyte/dendritic cell molecular signature of SARS-CoV-2-related multisystem inflammatory syndrome in children with severe myocarditis.Med (New York, N.Y.) · 2021Article
- Inhibition of TNFR1 Attenuates LPS Induced Apoptosis and Inflammation in Human Nucleus Pulposus Cells by Regulating the NF-KB and MAPK Signalling Pathway.Neurochemical research · 2021Article
- FcRn is a CD32a coreceptor that determines susceptibility to IgG immune complex-driven autoimmunity.The Journal of experimental medicine · 2020Article
- The spinal microglial IL-10/β-endorphin pathway accounts for cinobufagin-induced mechanical antiallodynia in bone cancer pain following activation of α7-nicotinic acetylcholine receptors.Journal of neuroinflammation · 2020Article
- High-Dose Intravenous Immunoglobulins in the Treatment of Severe Acute Viral Pneumonia: The Known Mechanisms and Clinical Effects.Frontiers in immunology · 2020Review
- Intravenous immunoglobulin suppresses the polarization of both classically and alternatively activated macrophages.Human vaccines & immunotherapeutics · 2020Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Intravenous Immunoglobulin (IVIg) is used to treat autoimmune or inflammatory diseases, but its mechanism of action is not completely understood. We asked whether IVIg can induce interleukin-10 (IL-10) and reduce pro-inflammatory cytokine production in human monocytes, and whether this response is reduced in monocytes from people with an Fcγ receptor IIA (FcγRIIA) gene variant, which is associated with increased risk of inflammatory diseases and poor response to antibody-based biological therapy. IVIg increased IL-10 production and reduced pro-inflammatory cytokine production in response to bacterial lipopolysaccharide (LPS), which required FcγRI and FcγRIIB and activation of MAPKs, extracellular signal-regulated kinase 1/2 (ERK1/2), and p38. IL-10 production was lower and pro-inflammatory cytokine production was higher in monocytes from people with the FcγRIIA risk variant and the risk variant prevented IL-10 production in response to (IVIg+LPS). Finally, we show that IVIg did not induce MAPK activation in monocytes from people with the risk variant. Our results demonstrate that IVIg can skew human monocytes to an anti-inflammatory, IL-10-producing activation state, which is compromised in monocytes from people with the FcγRIIA risk variant. This research has profound implications for the use of IVIg because 25% of the population is homozygous for the FcγRIIA risk variant and its efficacy may be reduced in those individuals. In addition, this research may be useful to develop new therapeutic strategies to replace IVIg by cross-linking FcγRIs and FcγRIIBs to promote anti-inflammatory macrophage activation, independent of the FcγRIIA genotype.
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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.