ArticleEuropean journal of immunology2009
PI3K limits TNF-alpha production in CD16-activated monocytes.
Article in European journal of immunology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
11 citing papers in PubMed, 28 citations in OpenAlex.
- Clemastine ameliorates ulcerative colitis-induced cognitive impairment by restoring PI3K/Akt/GSK-3β signaling and suppressing ferroptosis.Inflammopharmacology · 2026Article
- Identification of a Novel Peptide fromFoods (Basel, Switzerland) · 2025Article
- Bioinformatics and systems biology approaches to identify molecular targeting mechanism influenced by COVID-19 on heart failure.Frontiers in immunology · 2022Article
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- Proinflammatory IgG Fc structures in patients with severe COVID-19.Nature immunology · 2021Article
- Cholesterol metabolism drives regulatory B cell IL-10 through provision of geranylgeranyl pyrophosphate.Nature communications · 2020Article
- Isolation Protocol of Mouse Monocyte-derived Dendritic Cells and Their Subsequent In Vitro Activation with Tumor Immune Complexes.Journal of visualized experiments : JoVE · 2018Article
- ERBB signaling attenuates proinflammatory activation of nonclassical monocytes.American journal of physiology. Heart and circulatory physiology · 2017Article
- The unique cytoplasmic domain of human FcγRIIIA regulates receptor-mediated function.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
- Phosphatidylinositol-3-kinase activity during in vitro dendritic cell generation determines suppressive or stimulatory capacity.Immunologic research · 2011Article
- CD16 (FcRgammaIII) as a potential marker of osteoclast precursors in psoriatic arthritis.Arthritis research & therapy · 2010Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
IgG complexes bind to Fc receptor family members FcgammaRI (CD64), FcgammaRII (CD32) and FcgammaRIII (CD16), activating cell MAPK and PI3K resulting in increased cytokine production from particular leukocytes. The signaling molecules involved in cytokine production after cross-linking CD16 have not been determined in monocytes. To address this question, TNF-alpha, IL-1beta and IL-6 were measured in activated monocytes after inhibiting MEK1/2, PI3K and glycogen synthase kinase-beta (GSK-3beta). The roles of GSK-3beta and NF-kappaB were then determined using reporter assays and siRNA treatment. The data suggested that an MAPK pathway stimulated TNF-alpha release but that active PI3K limited TNF-alpha, IL-1beta and IL-6 cytokine production after cross-linking CD16. PI3K was also shown to limit nuclear translocation of NF-kappaB. The limiting effect of PI3K on TNF-alpha production from activated monocytes depended on the decrease of GSK-3beta activity, which significantly reduced the transactivation of NF-kappaB. Moreover, the TNF-alpha production induced by CD16 cross-linking was reduced in monocytes after treatment with siRNA against NF-kappaB, implying that this transcription factor functioned in TNF-alpha production. The results suggest that CD16 cross-linking activated PI3K and that active PI3K limited TNF-alpha production by inhibiting GSK-3beta activity, that blocked the action of NF-kappaB.
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