ArticleThe American journal of pathology1996
Absence of exogenous interleukin-4-induced apoptosis of gingival macrophages may contribute to chronic inflammation in periodontal diseases.
Article in The American journal of pathology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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.
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Who cites it
12 citing papers in PubMed, 51 citations in OpenAlex.
- Phenotypic and Functional Alterations of Immune Effectors in Periodontitis; A Multifactorial and Complex Oral Disease.Journal of clinical medicine · 2021Article
- IL-4 gene polymorphisms and their relation to steroid-induced osteonecrosis of the femoral head in Chinese population.Molecular genetics & genomic medicine · 2019Article
- Immuno-pathogenesis of Periodontal Disease: Current and Emerging Paradigms.Current oral health reports · 2014Article
- Hyper-responsive phenotype in localized aggressive periodontitis.Journal of dental research · 2010Article
- Combined stimulation with the T helper cell type 2 cytokines interleukin (IL)-4 and IL-10 induces mouse mast cell apoptosis.The Journal of experimental medicine · 2000Article
- Serum immunoglobulin G (IgG) and IgG subclass responses to the RgpA-Kgp proteinase-adhesin complex of Porphyromonas gingivalis in adult periodontitis.Infection and immunity · 2000Article
- Targeted salivary gland immunization with plasmid DNA elicits specific salivary immunoglobulin A and G antibodies and serum immunoglobulin G antibodies in mice.Infection and immunity · 1999Article
- Alkaline conditions accelerate polymorphonuclear leukocyte apoptosis in vitro.Infection and immunity · 1999Article
- In vitro induction of activation-induced cell death in lymphocytes from chronic periodontal lesions by exogenous Fas ligand.Infection and immunity · 1999Article
- Direct activation of mast cells by prosthetic biomaterial particles.Journal of materials science. Materials in medicine · 1998Article
- A nontoxic mutant of cholera toxin elicits Th2-type responses for enhanced mucosal immunity.Proceedings of the National Academy of Sciences of the United States of America · 1997Article
- Mutants in the ADP-ribosyltransferase cleft of cholera toxin lack diarrheagenicity but retain adjuvanticity.The Journal of experimental medicine · 1997Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Inflamed gingival tissues are enriched in macrophages (MOs) and CD4-positive T cells; however, T helper-type cytokines such as interleukin (IL)-2 and IL-4 are absent. Therefore, we investigated whether a relationship exists between IL-4 receptor (IL-4R) expression and MO persistence in the absence of exogenous IL-4. Gingival MOs, when compared with monocyte(MN)/MOs from peripheral blood mononuclear cells, expressed high levels of IL-4R mRNA. Furthermore, in vitro cultures of gingival MOs remained viable whereas identically treated peripheral blood MN/MOs rapidly lost viability. However, when gingival MOs were incubated with recombinant IL-4 (rIL-4), the cell viability was dramatically reduced. When the frequency of apoptotic cells was assessed in rIL-4-treated gingival MO cultures, higher numbers of apoptotic cells were noted in rIL-4-treated versus control cultures. Furthermore, rIL-4-treated MOs from inflamed gingiva showed DNA fragmentation as assessed by electrophoresis. These findings clearly show that addition of exogenous rIL-4 to gingival MO cultures leads to cell death by apoptosis. This finding would suggest that topical application of rIL-4 may inhibit the persistence of MOs in adult periodontitis, which could then lead to decreased inflammation.
Indexed as
Identifiers
8546223PMC1861600W174603300What OpenQuestion holds
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.