ArticleClinical and experimental immunology1994
Cytokine regulation of low-affinity IgE receptor (CD23) on monocytes from asthmatic subjects.
Article in Clinical and experimental immunology, 1994. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
2 citing papers in PubMed, 7 citations in OpenAlex.
- CD23 surface density on B cells is associated with IgE levels and determines IgE-facilitated allergen uptake, as well as activation of allergen-specific T cells.The Journal of allergy and clinical immunology · 2017Article
- Recombinant IgE antibodies for passive immunotherapy of solid tumours: from concept towards clinical application.Cancer immunology, immunotherapy : CII · 2012Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The regulation of CD23 expression (Fc epsilon RII) by cytokines on monocytes from normal subjects, asymptomatic and acute asthmatics was investigated. CD23 was weakly expressed on cells from controls, but was significantly enhanced in the two groups of asthmatics. The addition of IL-4 on monocytes induced an increase of CD23 expression in cells from controls and asthmatics. Interferon-gamma (IFN-gamma) did not modulate CD23 expression in asthmatics or control subjects, while high doses of IL-6 (2000 U/ml) enhanced CD23 expression on cells from asthmatics or controls. In vitro stimulation of monocytes with Timothy grass pollen allergen did not enhance CD23 receptor in asthmatics with a positive skin test to this pollen. We speculate that CD23 expression in asthmatics is markedly enhanced by Th2-dependent cytokines, such as IL-4 and IL-6. Thus, the regulation of Th2 cell activation by anti-cytokine therapy could have an important effect on the down-regulation of CD23 on monocytes, and in shifting a Th2 subpopulation into a Th1 subpopulation by blocking Th2-dependent cytokines.
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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.