ArticleAnnals of the rheumatic diseases2003
Immune complexes from SLE sera induce IL10 production from normal peripheral blood mononuclear cells by an FcgammaRII dependent mechanism: implications for a possible vicious cycle maintaining B cell hyperactivity in SLE.
Article in Annals of the rheumatic diseases, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It is linked to trial NCT02455089 (Prognosis Assessment of the Increase of GADD34 Gene Expression for Patient Suffering From Systemic Lupus Erythematosus), which is not on this map. Cited by 43 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
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.
Prognosis Assessment of the Increase of GADD34 Gene Expression for Patient Suffering From Systemic Lupus Erythematosus
Who cites it
43 citing papers in PubMed, 134 citations in OpenAlex.
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- Clinical Proteomics Profiling for Biomarker Identification Among Patients Suffering With Indian Post Kala Azar Dermal Leishmaniasis.Frontiers in cellular and infection microbiology · 2020Article
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- Lupus-like Disease in FcγRIIBScientific reports · 2019Article
- Kawasaki Disease: The Role of Immune Complexes Revisited.Frontiers in immunology · 2019Review
- The Human FcγRII (CD32) Family of Leukocyte FcR in Health and Disease.Frontiers in immunology · 2019Review
- Immune complexes containing scleroderma-specific autoantibodies induce a profibrotic and proinflammatory phenotype in skin fibroblasts.Arthritis research & therapy · 2018Article
- Mass cytometry identifies a distinct monocyte cytokine signature shared by clinically heterogeneous pediatric SLE patients.Journal of autoimmunity · 2017Article
- Immunomodulators in SLE: Clinical evidence and immunologic actions.Journal of autoimmunity · 2016Review
- Small amounts of sub-visible aggregates enhance the immunogenic potential of monoclonal antibody therapeutics.Pharmaceutical research · 2015Article
- Sera from patients with active systemic lupus erythematosus patients enhance the toll-like receptor 4 response in monocyte subsets.Journal of inflammation (London, England) · 2015Article
- Pathologic patterns of interleukin 10 expression--a review.Biochemia medica · 2015Review
- Normal serum levels of immune complexes in postpolio patients.Results in immunology · 2014Article
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundRaised interleukin (IL)6 and IL10 levels are thought to contribute to the pathogenesis of systemic lupus erythematosus (SLE) by enhancing autoantibody production and immune complex (IC) formation. These immune complexes can then stimulate cellular reactions through Fc and complement receptors.
objectiveTo investigate whether circulating SLE ICs stimulate type 2 cytokine production.
methodsTwenty serum samples from patients with active SLE were compared with sera from 18 healthy controls. Sera and polyethylene glycol (PEG) precipitates from sera were added to peripheral blood mononuclear cell (PBMC) cultures, and the production of IL10 and IL6 was investigated by enzyme linked immunospot assay (ELISPOT) and enzyme linked immunosorbent assay (ELISA). Fc gamma receptor (FcgammaR) antibodies were used in blocking experiments, and flow cytometry was used to assess the correlation between monocyte FcgammaR expression and IC-induced cytokine production.
resultsTen per cent dilutions of the SLE sera induced a significantly increased number of IL10-producing cells in comparison with control sera (median, 11.75 v 1.25 spot forming cells/50 000 PBMC; p<0.0001). PEG precipitates from SLE sera also induced significantly increased levels of IL10 (p=0.016) and IL6 (p=0.042) in comparison with control PEG precipitates. IL10 production induced by SLE PEG precipitates or by artificial ICs could be blocked by anti-FcgammaRII antibodies, and the FcgammaRII expression on CD14+ monocytes correlated with the IC-induced production of IL10 and IL6.
conclusionsSLE sera stimulate IL10 and IL6 production from PBMC, and this effect is at least partly explained by precipitable ICs acting through FcgammaRII. This effect provides a possible mechanism for the enhanced production of IL10 in SLE, whereby B cell activation, antibody production, IC stimulated monocytes/macrophages, and type 2 cytokines create a vicious cycle that may help to maintain B cell hyperactivity in SLE.
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