Mast cells: function and contents

Schwartz, Lawrence B.

doi:10.1016/0952-7915(94)90039-6

Cited by 191 publications

(106 citation statements)

References 37 publications

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“…These conditions are often triggered by FcεRI-mediated signals in mast cells (1,2). Thus, the inhibition of FcεRI has led to various therapeutic approaches for allergies.…”

Section: Discussionmentioning

confidence: 99%

“…Activation of FcεRI activates several signaling pathways, which leads to degranulation and release of histamine (1). The tyrosine kinases, including Lyn, Fyn, and Syk, are involved in initiating the assembly of large signaling complexes (2,3).…”

Section: Discussionmentioning

confidence: 99%

“…They constitutively express the high-affinity IgE receptor, FcεRI, on their surface (1,2). Aggregation of FcεRI eventually leads to the release of granule components such as histamine and the change in adhesive property, cell shape, and surface topography, as well as the de novo synthesis of lipid mediators and cytokines (3).…”

mentioning

confidence: 99%

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Signal-Transducing Adaptor Protein-2 Controls the IgE-Mediated, Mast Cell–Mediated Anaphylactic Responses

Sekine

Nishida

Yamasaki

et al. 2014

The Journal of Immunology

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Signal-transducing adaptor protein-2 (STAP-2) is a recently identified adaptor protein that regulates immune and inflammatory responses through interactions with a variety of signaling and transcriptional molecules. In the current study, we clarified the physiological role of STAP-2 in mast cell function, a key mediator of IgE-associated allergic responses. STAP-2 is constitutively expressed in mast cells. STAP-2 deficiency in mast cells greatly enhances FcεRI-mediated signals, resulting in the increased tyrosine phosphorylation of the phospholipase C-γ isoform, calcium mobilization, and degranulation. Of importance, STAP-2–deficient mice challenged with DNP-BSA after passive sensitization with anti-DNP IgE show more severe rectal temperature decrease than do wild-type mice. STAP-2–deficient mice also show increased vascular permeability and more severe cutaneous anaphylaxis after DNP-BSA injection. These regulatory functions performed by STAP-2 indicate that there is an interaction between STAP-2 and FcεRI. In addition, our previous data indicate that STAP-2 binds to the phospholipase C-γ isoform and IκB kinase-β. Therefore, our data described in this article strongly suggest that manipulation of STAP-2 expression in mast cells may control the pathogenesis of allergic diseases and have the potential for treating patients with allergy.

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“…These conditions are often triggered by FcεRI-mediated signals in mast cells (1,2). Thus, the inhibition of FcεRI has led to various therapeutic approaches for allergies.…”

Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Signal-Transducing Adaptor Protein-2 Controls the IgE-Mediated, Mast Cell–Mediated Anaphylactic Responses

Sekine

Nishida

Yamasaki

et al. 2014

The Journal of Immunology

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“…Nevertheless, mast cell tissue-dependent differentiation is reversible; fibroblast-derived factors change mucosal type mast cells into serosal ones, whereas IL-3 favors the mucosal phenotype (1,6). Besides tissue distribution, life span and mediator content of their intracellular granules are also different (5).…”

mentioning

confidence: 99%

“…Clustering of type I Fc⑀R (Fc⑀RI) 4 present in their plasma membrane initiates a coupling cascade culminating in the secretion of inflammatory mediators, including histamine, serotonin, proteases, leukotrienes, and several cytokines (1). Lyn, a src family protein tyrosine kinase (PTK) interacts with the ␤ subunit of the receptor complex and undergoes phosphorylation and activation as a result of Fc⑀RI clustering.…”

mentioning

confidence: 99%

The β Subunit of the Type I Fcε Receptor Is a Target for Peptides Inhibiting IgE-Mediated Secretory Response of Mast Cells

Andrásfalvy

Péterfy²,

Tóth

et al. 2005

The Journal of Immunology

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Peptides originally derived from complement component C3a were earlier shown to inhibit the type I FcεR (FcεRI)-mediated degranulation of mucosal type mast cells. In the present study, we show that C3a7, a peptide with a natural sequence, and its modified derivative, C3a9, are powerful inhibitors of the above response of both serosal and mucosal type mastocytes. We demonstrate that these peptides inhibit FcεRI-induced membrane proximal events, suppress phosphorylation of the FcεRI β subunit, the protein tyrosine kinase Lyn, as well as the transient rise in free cytosolic Ca2+ level. The late phase of cellular response was also inhibited, as demonstrated by the reduced TNF-α secretion. Experiments using two independent methods provided evidence that the interaction site of complement-derived peptides is the FcεRI β-chain. This was further supported by fluorescence confocal microscopic colocalization and resonance energy transfer measurements. Taken together, these results suggest the presence of distinct “activating” and “inhibitory” motifs in the C3a sequence. Response to both is in balance under physiologic conditions. Furthermore, present data predict that such inhibitory peptides may serve as potent agents for future therapeutic intervention.

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H1 and H2 histamine receptors modulate osteoclastic resorption by different pathways: Evidence obtained by using receptor antagonists in a rat synchronized resorption model

Dobigny

Saffar

1997

J. Cell. Physiol.

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We have previously postulated that mast cells (MC) may act as accessory cells in bone resorption. In this study we obtained evidence that histamine, the most abundant mediator released upon MC degranulation, is one of many factors modulating resorption. As the effect of histamine is mediated through different receptors, we tested the effects of mepyramine (1.5 mg/kg/day) and cimetidine (125 mg/kg/day), that antagonize H1 and H2 receptors, respectively. These effects were assessed morphometrically in a well-defined rat model of synchronized resorption at different stages of the process. On day 4 after induction (i.e., at the peak of resorption in this model), both agents reduced resorption significantly. Mepyramine acted by disturbing osteoclast activation and by reducing osteoclast activity (P < 0.01), while cimetidine principally reduced the size of the osteoclast population (P < 0.01). On day 6 (stage of declining resorption), the same resorption score as on day 4 was maintained in the mepyramine group, mainly through a marked increase in osteoclast activity (P < 0.01). In contrast, cimetidine continued to strongly reduce resorption (P < 0.01) and led to a further drop in the osteoclast population (P < 0.01). One day after induction, nonspecific esterase (NSE)-positive cells (putative osteoclast precursors) were significantly less numerous after treatment with the two agents. Significant changes in the MC population in the vicinity of the zone undergoing resorption occurred on days 4 and 6. The periosteal microvasculature adjacent to the reference bone zone was also markedly modified, especially in the cimetidine group. These results show that histamine intervenes in resorption through both H1 and H2 receptors. However, the mechanisms triggered by these receptors were quite different: H2 receptors appeared to be more strategic, as no replenishment of the osteoclast population occurred after the initial depletion in precursors. Histamine also appears to influence other neighbouring compartments, in which disturbances are probably linked to defective resorption. These findings support our hypothesis by which MC are accessory cells of resorption in this model.

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Mast cells: function and contents

Cited by 191 publications

References 37 publications

Signal-Transducing Adaptor Protein-2 Controls the IgE-Mediated, Mast Cell–Mediated Anaphylactic Responses

Signal-Transducing Adaptor Protein-2 Controls the IgE-Mediated, Mast Cell–Mediated Anaphylactic Responses

The β Subunit of the Type I Fcε Receptor Is a Target for Peptides Inhibiting IgE-Mediated Secretory Response of Mast Cells

H1 and H2 histamine receptors modulate osteoclastic resorption by different pathways: Evidence obtained by using receptor antagonists in a rat synchronized resorption model

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