IL-4 upregulates FcϵRI α-chain messenger RNA in eosinophils

Terada, Nobuhisa; Konno, Akira; Terada, Yasuhiko; Fukuda, Setsuya; Yamashita, Tatsuhisa; Abe, Tomiya; Shimada, Hideaki; Ishida, Kazuhiro; Yoshimura, Kazuya; Tanaka, Yoïchi

doi:10.1016/s0091-6749(95)70201-6

Cited by 57 publications

(33 citation statements)

References 17 publications

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“…Indeed, preliminary data from our laboratory revealed that incubation of ASM cells with various IgE concentrations results in Fc⑀RI ␣-chain mRNA up-regulation (data not shown). Furthermore, Th2 cytokines, particularly IL-4, have been shown to play a positive role on the transcription of Fc⑀RI ␣-chain in human mast cells (29,30), human eosinophils obtained from atopic dermatitis subjects (31), and in dendritic cells (32). Whether a similar effect occurs in ASM cells is unknown.…”

Section: )mentioning

confidence: 99%

Human Airway Smooth Muscle Cells Express the High Affinity Receptor for IgE (FcεRI): A Critical Role of FcεRI in Human Airway Smooth Muscle Cell Function

Gounni

Wellemans

Yang

et al. 2005

The Journal of Immunology

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Several reports suggest that activated airway smooth muscle (ASM) cells are capable of generating various proinflammatory mediators, including cytokines and chemokines. However, little is known about the mechanism involved in this process. In this regard, we have examined the expression and the role of the high affinity IgE receptor (FcεRI) by ASM cells. Human ASM cells were found to constitutively express transcripts coding for α, β, and γ subunits of FcεRI. Flow cytometry and Western blot analysis confirmed the expression of FcεRI α-chain protein. Interestingly, FcεRI α-chain immunoreactivity was also demonstrated in smooth muscle within bronchial biopsies of asthmatic subjects. Cross-linking of FcεRI induced mobilization of free calcium in ASM cells, one of the critical signals to trigger smooth muscle contraction. Furthermore, cultured ASM cells released IL-4, IL-13, IL-5, and eotaxin but not IFN-γ, when sensitized with IgE followed by anti-IgE Ab cross-linking. The addition of anti-FcεRI α-chain Abs directed against IgE binding site inhibited this release. Taken together, these results suggest a potential new and important mechanism by which ASM cells may participate in airway inflammation and bronchoconstriction associated with allergic asthma.

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Section: )mentioning

confidence: 99%

Human Airway Smooth Muscle Cells Express the High Affinity Receptor for IgE (FcεRI): A Critical Role of FcεRI in Human Airway Smooth Muscle Cell Function

Gounni

Wellemans

Yang

et al. 2005

The Journal of Immunology

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“…Mast cells from IgE-deficient mice express low levels of Fc⑀RI, which suggests that the basal levels are under the control of other mechanisms (111). Cytokines, particularly IL-4, have been shown to play a positive role in the transcription of Fc⑀RI ␣-chain in human mast cells (106), human eosinophils from atopic dermatitis subjects (104), and human dendritic cells (30). In mice, however, IL-4 and also IL-10 decrease Fc⑀RI expression specifically affecting FcR ␤-, but not FcR ␣-or FcR ␥-, subunits (32,93).…”

Section: Fc⑀ri Regulationmentioning

confidence: 99%

The high-affinity IgE receptor (FcεRI): a critical regulator of airway smooth muscle cells?

Gounni

2006

American Journal of Physiology-Lung Cellular and Molecular Phys

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“…In the former case, IgE is not the only factor that is likely to promote Fc⑀RI expression over such an extended period; IL-4 is another one (24,(41)(42)(43). A similar phenomenon had been observed on intestinal rat mast cells, where infection by Nippostrongylus brasiliensis was more efficient at increasing Fc⑀RI expression (measured by detection of FcR␤) than the mere injection of IgE (44).…”

Section: Figurementioning

confidence: 99%

Human Eosinophils and Human High Affinity IgE Receptor Transgenic Mouse Eosinophils Express Low Levels of High Affinity IgE Receptor, but Release IL-10 upon Receptor Activation

Kayaba

Dombrowicz

Woerly

et al. 2001

The Journal of Immunology

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FcεRI expressed by human eosinophils is involved in IgE-mediated cytotoxicity reactions toward the parasite Schistosoma mansoni in vitro. However, because receptor expression is low on these cells, its functional role is still controversial. In this study, we have measured surface and intracellular expression of FcεRI by blood eosinophils from hypereosinophilic patients and normal donors. The number of unoccupied receptors corresponded to ∼4,500 Ab binding sites per cell, whereas 50,000 Ab binding sites per cell were detected intracellularly. Eosinophils from patients displayed significantly more unoccupied receptors than cells from normal donors. This number correlated to both serum IgE concentrations and to membrane-bound IgE. The lack of FcεRI expression by mouse eosinophils has hampered further studies. To overcome this fact and experimentally confirm our findings on human eosinophils, we engineered IL-5 × hFcεRIα double-transgenic mice, whose bone marrow, blood, spleen, and peritoneal eosinophils expressed FcεRI levels similar to levels of human eosinophils, after 4 days culture with IgE in the presence of IL-5. Both human and mouse eosinophils were able to secrete IL-10 upon FcεRI engagement. Thus, comparative analysis of cells from patients and from a relevant animal model allowed us to clearly demonstrate that FcεRI-mediated eosinophil activation leads to IL-10 secretion. Through FcεRI expression, these cells are able to contribute to both the regulation of the immune response and to its effector mechanisms.

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IL-4 upregulates FcϵRI α-chain messenger RNA in eosinophils

Cited by 57 publications

References 17 publications

Human Airway Smooth Muscle Cells Express the High Affinity Receptor for IgE (FcεRI): A Critical Role of FcεRI in Human Airway Smooth Muscle Cell Function

Human Airway Smooth Muscle Cells Express the High Affinity Receptor for IgE (FcεRI): A Critical Role of FcεRI in Human Airway Smooth Muscle Cell Function

The high-affinity IgE receptor (FcεRI): a critical regulator of airway smooth muscle cells?

Human Eosinophils and Human High Affinity IgE Receptor Transgenic Mouse Eosinophils Express Low Levels of High Affinity IgE Receptor, but Release IL-10 upon Receptor Activation

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