Expression of functional high affinity immunoglobulin E receptors (Fc epsilon RI) on monocytes of atopic individuals.

Maurer, Dieter; Fiebiger, Edda; Reininger, Bärbel; Wolff‐Winiski, Barbara; Jouvin, Marie-Hélène; Kilgus, Oliver; Kinét, Jean-Pierre; Stingl, Georg

doi:10.1084/jem.179.2.745

Cited by 353 publications

(257 citation statements)

References 19 publications

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“…FcεRI is expressed in limited types of cells such as mast cells, basophils, eosinophils [1], monocytes [2], Langerhans cells [3,4], platelets [5,6] and neutrophils [7]. Cross-linking of FcεRI on effector cells by antigen (allergen)-IgE complexes induces not only the release of chemical mediators in the early-phase reaction but also cytokine gene expressions, leading to the late-phase reaction.…”

Section: Introductionmentioning

confidence: 99%

“…Although a functional receptor is expressed both as a tetramer (αβγ 2 ) and a trimer (αγ 2 ) in humans [8], intracellular signals [9,10] in addition to cell-surface expression [11] have been reported to be amplified significantly by the β-chain, indicating that the β-chain increases the sensitivity of cell activation to stimulation by allergens. Therefore functional inhibition of the β-chain is a reasonable strategy to suppress allergic reaction by raising the threshold of FcεRI-mediated cell activation by decreasing both the intracellular signals and the cell-surface FcεRI expression.…”

Section: Introductionmentioning

confidence: 99%

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FHL3 negatively regulates human high-affinity IgE receptor β-chain gene expression by acting as a transcriptional co-repressor of MZF-1

Takahashi

Matsumoto

2005

Biochemical Journal

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The high-affinity IgE receptor FcεRI plays a key role in triggering allergic reactions. We recently reported that human FcεRI β-chain gene expression was down-regulated by a transcription factor, MZF-1, through an element in the fourth intron. In the present study, we found that this transcriptional repression by MZF-1 required FHL3 (four and a half LIM domain protein 3) as a cofactor. Yeast two-hybrid and immunoprecipitation assays demonstrated that FHL3 bound MZF-1 in vitro and in vivo. Overexpression of FHL3 in KU812 cells suppressed the β-chain promoter activity through the element in the fourth intron in an MZF-1-dependent manner. Furthermore, results from pull-down assays and gel-filtration chromatography employing nuclear extracts indicated that MZF-1 and FHL3 formed a complex of high molecular mass with some additional proteins in the nucleus. Granulocyte-macrophage colony-stimulating factor, which was reported to decrease FcεRI expression, induced the accumulation of FHL3 in the nucleus, in accordance with the repressive role of FHL3 in β-chain gene expression.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

FHL3 negatively regulates human high-affinity IgE receptor β-chain gene expression by acting as a transcriptional co-repressor of MZF-1

Takahashi

Matsumoto

2005

Biochemical Journal

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“…Immunoblotting was performed, as described (32). Blotted samples were probed with first-step reagents (anti-Cdc42, anti-Rac1, anti-MHC class I H chain, or anti-CD59), followed by HRP-coupled goat anti-mouse IgG (BioRad) and West Pico luminescent reagent (Pierce, Rockford, IL).…”

Section: Sds-page and Western Blottingmentioning

confidence: 99%

Lipid Raft-Associated GTPase Signaling Controls Morphology and CD8+ T Cell Stimulatory Capacity of Human Dendritic Cells

Jaksits

Bauer

Kriehuber

et al. 2004

The Journal of Immunology

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Their eponymous morphology and unique ability to activate naive T cells are hallmark features of dendritic cells (DCs). Specific properties of the actin cytoskeleton may define both characteristics. In search for regulators that coordinate DC phenotype and function, we observed strongly increased expression of the actin-remodeling GTPases Cdc42 and Rac1 during DC development from human stem cells. Cdc42 and Rac1 are constitutively active in immature DCs, and their activity is further up-regulated by maturational stimuli such as LPS or CD40L. Activation of Rac1 is associated with its rapid recruitment into lipid rafts. Cdc42 is not recruited into rafts, but readily activated by raft-associated moieties. The functional interplay of rafts, GTPases, and cortical actin is further shown by GTPase activation and actin remodeling after pharmacological disruption of lipid rafts and by the loss of the actin-based DC morphology by transfection of dominant-negative Cdc42 and Rac1. Both Cdc42 and Rac1 also control the transport of essential immunostimulatory molecules to the DC surface. Transfection with dominant-negative GTPases led to reduced surface expression of MHC class I and CD86. Consecutively, DCs display a reduced stimulatory capacity for CD8+ T cells, whereas MHC class II-dependent stimulation of CD4+ T cells remains unperturbed. We conclude that Cdc42 and Rac1 signaling controls DC morphology and conditions DCs for efficient CD8+ T cell stimulation.

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“…As a consequence, FcεRI can be expressed in human mast cells with or without FcRβ. They can also be expressed by human monocytes, macrophages and eosinophils, which do not express FcRβ (Maurer et al, 1994), but not in corresponding murine cells. Signals triggered by FcRβ-associated FcεRI were found to be of a higher intensity than signals triggered by FcεRI associated with FcRγ only (Dombrowicz et al, 1998).…”

Section: Fcrβmentioning

confidence: 99%

Negative Signaling in Fc Receptor Complexes

Daëron

Lesourne

2006

Advances in Immunology

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Cell activation results from the transient displacement of an active balance between positive and negative signaling. This displacement depends in part on the engagement of cell surface receptors by extracellular ligands. Among these are Receptors for the Fc portion of immunoglobulins (FcRs). FcRs are widely expressed by cells of hematopoietic orign. When binding antibodies, FcRs provide these cells with immunoreceptors capable of triggering numerous biological responses in response to specific antigen. FcR-dependent cell activation is regulated by negative signals which are generated together with positive signals within signalosomes that form upon FcR engagement. Many molecules involved in positive signaling, including the FcRβ subunit, the src kinase lyn, the cytosolic adapter Grb2, the transmembrane adapters LAT and NTAL, are indeed also involved in negative signaling. A major player in negative regulation of FcR signaling is the inositol 5-phosphatase SHIP1. Several layers of negative regulation operate sequentially as FcRs are engaged by extracellular ligands of increasing valency. A background protein tyrosine phosphatasedependent negative regulation maintains cells in a « resting » state. SHIP1-dependent negative regulation can be detected as soon as high-affinity FcRs are occupied by antibodies in the absence of antigen. It increases when activating FcRs are engaged by multivalent ligands and, further when FcR aggregation increases, accounting for the bell-shaped dose-response curve observed in excess of ligand. Finally, F-actin skeleton-associated high-molecular weight SHIP1, recruited to phopshorylated ITIMs, concentrates in signaling complexes when activating FcRs are coengaged with inhibitory FcRs by immune complexes. Based on these data, activating and inhibitory FcRs could be used for new therapeutic approaches of immune disorders.

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Expression of functional high affinity immunoglobulin E receptors (Fc epsilon RI) on monocytes of atopic individuals.

Cited by 353 publications

References 19 publications

FHL3 negatively regulates human high-affinity IgE receptor β-chain gene expression by acting as a transcriptional co-repressor of MZF-1

FHL3 negatively regulates human high-affinity IgE receptor β-chain gene expression by acting as a transcriptional co-repressor of MZF-1

Lipid Raft-Associated GTPase Signaling Controls Morphology and CD8+ T Cell Stimulatory Capacity of Human Dendritic Cells

Negative Signaling in Fc Receptor Complexes

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