ArticleThe Journal of clinical investigation2000
The high-affinity IgE receptor (FcepsilonRI) blocks apoptosis in normal human monocytes.
Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 86 citations in OpenAlex.
- CD2 identifies a monocyte subpopulation with immunoglobulin E-dependent, high-level expression of Fc epsilon RI.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2006Trial
- Review
- Observational
- The role of FcεRI expressed in dendritic cells and monocytes.Cellular and molecular life sciences : CMLS · 2015Review
- IgE actions on CD4+ T cells, mast cells, and macrophages participate in the pathogenesis of experimental abdominal aortic aneurysms.EMBO molecular medicine · 2014Article
- Article
- IgE induces proliferation in human airway smooth muscle cells: role of MAPK and STAT3 pathways.Allergy, asthma, and clinical immunology : official journal of the Canadian Society of Allergy and Clinical Immunology · 2013Article
- Increased plasma LIGHT levels in patients with atopic dermatitis.Clinical and experimental immunology · 2012Article
- The serine protease plasmin triggers expression of the CC-chemokine ligand 20 in dendritic cells via Akt/NF-κB-dependent pathways.Journal of biomedicine & biotechnology · 2012Article
- IgE stimulates human and mouse arterial cell apoptosis and cytokine expression and promotes atherogenesis in Apoe-/- mice.The Journal of clinical investigation · 2011Article
- Article
- Article
- Exosomes released from infected macrophages contain Mycobacterium avium glycopeptidolipids and are proinflammatory.The Journal of biological chemistry · 2007Article
- Effect of serotonin on the differentiation of human monocytes into dendritic cells.Clinical and experimental immunology · 2006Article
- The immunoglobulin E receptor: expression and regulation.Current allergy and asthma reports · 2005Review
- Immunoglobulin E-bearing antigen-presenting cells in atopic dermatitis.Current allergy and asthma reports · 2004Review
- Redox status and immune function in type I diabetes families.Clinical and experimental immunology · 2004Article
- Quantification of indoleamine 2,3-dioxygenase gene induction in atopic and non-atopic monocytes after ligation of the high-affinity receptor for IgE, Fc(epsilon)RI and interferon-gamma stimulation.Clinical and experimental immunology · 2003Article
- MCL1 provides a window on the role of the BCL2 family in cell proliferation, differentiation and tumorigenesis.Leukemia · 2002Review
- Why is the prevalence of allergic diseases increasing? A critical assessment of some classical risk factors.Mediators of inflammation · 2001Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Monocytes have a limited life span, and their homeostasis is regulated by apoptosis in vivo. When cultured in the absence of appropriate exogenous stimuli, they undergo apoptosis, but under the influence of survival signals, these cells differentiate into macrophages or dendritic cells. Here we show that ligation of the high-affinity IgE receptor (FcepsilonRI) on human monocytes from nonatopic individuals markedly reduces apoptosis induced by serum deprivation or by CD95/Fas ligation. Aggregation of FcepsilonRI reduces its own expression but fails to modulate CD95/Fas expression. In contrast, FcepsilonRI ligation enhances the expression of the antiapoptotic molecules Bcl-2 and Bcl-xL, but not Mcl-1, in monocytes. Incubation of unstimulated cells with culture supernatants of FcepsilonRI-activated monocytes prolongs their life span, whereas CD95/Fas expression remains unaffected. The incidence of apoptosis is restored considerably when the supernatant is depleted of TNF-alpha, whereas elimination of IL-1beta, GM-CSF, or IL-12 has no effect. These results indicate that FcepsilonRI mediates signals preventing monocyte apoptosis directly by increasing the levels of Bcl-2 and Bcl-xL, and indirectly by means of TNF-alpha in an autocrine and paracrine fashion. This process may contribute to the establishment of chronic allergic disorders such as atopic dermatitis.
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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.