Human Cardiac Mast Cells and Their Role in Severe Allergic Reactions

1998 ◽  
pp. 237-257 ◽  
Author(s):  
Gianni Marone ◽  
Gennaro De Crescenzo ◽  
Vincenzo Patella ◽  
Arturo Genovese
Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1615
Author(s):  
Zhongwei Zhang ◽  
Yosuke Kurashima

It is well known that mast cells (MCs) initiate type I allergic reactions and inflammation in a quick response to the various stimulants, including—but not limited to—allergens, pathogen-associated molecular patterns (PAMPs), and damage-associated molecular patterns (DAMPs). MCs highly express receptors of these ligands and proteases (e.g., tryptase, chymase) and cytokines (TNF), and other granular components (e.g., histamine and serotonin) and aggravate the allergic reaction and inflammation. On the other hand, accumulated evidence has revealed that MCs also possess immune-regulatory functions, suppressing chronic inflammation and allergic reactions on some occasions. IL-2 and IL-10 released from MCs inhibit excessive immune responses. Recently, it has been revealed that allergen immunotherapy modulates the function of MCs from their allergic function to their regulatory function to suppress allergic reactions. This evidence suggests the possibility that manipulation of MCs functions will result in a novel approach to the treatment of various MCs-mediated diseases.


2021 ◽  
Vol 11 ◽  
Author(s):  
Rosa Muñoz-Cano ◽  
Clara San Bartolome ◽  
Rocío Casas-Saucedo ◽  
Giovanna Araujo ◽  
Sonia Gelis ◽  
...  

Cofactors may explain why in some cases food ingestion leads to anaphylaxis while in others elicits a milder reaction or tolerance. With cofactors, reactions become more severe and/or have a lower allergen threshold. Cofactors are present in up to 58% of food anaphylaxis (FAn). Exercise, NSAIDs, and alcohol are the most frequently described, although the underlying mechanisms are poorly known. Several hypotheses have suggested the influence of these cofactors on basophils and mast cells (MCs). Exercise has been suggested to enhance MC activation by increasing plasma osmolarity, redistributing blood flow, and activating adenosine and eicosanoid metabolism. NSAIDs’ cofactor effect has been related with cyclooxygenase inhibition and therefore, prostaglandin E2 (PGE2) production. Indeed, overexpression of adenosine receptor 3 (A3) gene has been described in NSAID-dependent FAn; A3 activation potentiates FcϵRI-induced MC degranulation. Finally, alcohol has been related with an increase of histamine levels by inhibition of diamino oxidase (DAO) and also with and increase of extracellular adenosine by inhibition of its uptake. However, most of these mechanisms have limited evidence, and further studies are urgently needed. In conclusion, the study of the immune-related mechanisms involved in food allergic reactions enhanced by cofactors is of the utmost interest. This knowledge will help to design both tailored treatments and prophylactic strategies that, nowadays, are non-existent.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Hae Mi Joo ◽  
Eun Hee Hong ◽  
Seong-Jun Cho ◽  
Seon Young Nam ◽  
Ji Young Kim

Abstract The prevalence of allergies has increased over the last four decades. In allergic reactions, mast cells induce a hypersensitive immune response to a substance that is normally harmless. Ionizing radiation has different biological effects depending on the dose and dose rate. In this study, we investigated whether low-dose irradiation before (preventative effect) or after (therapeutic effect) an antigen-antibody reaction has an anti-allergic effect. To test this, we activated rat basophilic leukemia (RBL-2H3) mast cells with anti-2,4-dinitrophenyl IgE (antibody) and 2,4-dinitrophenyl human serum albumin, which served as an antigen. To test for both the potential of a preventative effect and a therapeutic effect, we irradiated mast cells both before and after mast cell activation, and we measured mediator release and signaling pathway activity. Low-dose ionizing radiation suppressed mediator release from RBL-2H3 mast cells activated by the antigen-antibody reaction regardless of when the mast cells were irradiated. These results were due to the suppression of FcεRI expression. Therefore, we suggest that low-dose ionizing radiation has a preventative and therapeutic effect in allergic reactions via the FcεRI-mediated RBL-2H3 mast cell activation system.


2019 ◽  
Vol 2019 ◽  
pp. 1-8
Author(s):  
Hyun Ju Do ◽  
Tae Woo Oh ◽  
Kwang-Il Park

This study is aimed at determining whether Sesamum indicum Linn. beneficially influences FcεRI-mediated allergic reactions in RBL-2H3 mast cells; it is also aimed at further investigating Lyn/Fyn and Syk signaling pathways. To examine the antiallergic effect of Sesamum indicum Linn. extract (SIE), we treated antigen/immunoglobulin E- (IgE-) sensitized mast cells with extracts of various concentrations. We examined the degranulation release and concentrations of inflammatory mediators. Additionally, the expressions of genes involved in the FcεRI and arachidonate signaling pathways were examined. SIE inhibited the degranulation and secretion of inflammatory mediators in antigen/IgE-sensitized mast cells. SIE reduced the expressions of FcεRI signaling-related genes, such as Syk, Lyn, and Fyn, and the phosphorylation of extracellular signal-regulated kinase in antigen/IgE-sensitized mast cells. Additionally, in late allergic responses, SIE reduced PGD2 release and COX-2 and cPLA2 phosphorylation expression in FcεRI-mediated mast cell activation. Lastly, 250–500 mg/kg SIE significantly attenuated the Ag/IgE-induced passive cutaneous anaphylaxis (PCA) reaction in mice. The potent effect of SIE on RBL-2H3 mast cell activation indicates that the extract could potentially be used as a novel inhibitor against allergic reactions.


2019 ◽  
Vol 20 (15) ◽  
pp. 3701 ◽  
Author(s):  
Theoharis C. Theoharides ◽  
Irene Tsilioni ◽  
Pio Conti

Mast cells are unique immune cells involved in allergic reactions, but also in immunity and inflammation. Interleukin 37 (IL-37) has emerged as an important regulatory cytokine with ability to inhibit immune and inflammatory processes. IL-37 is made primarily by macrophages upon activation of toll-like receptors (TLR) leading to generation of mature IL-37 via the action of caspase 1. In this review, we advance the premise that mast cells could regulate the anti-inflammatory activity of the IL-37 via their secretion of heparin and tryptase. Extracellular IL-37 could either dimerize in the presence of heparin and lose biological activity, or be acted upon by proteases that can generate even more biologically active IL-37 forms. Molecules that could selectively inhibit the secretion of mast cell mediators may, therefore, be used together with IL-37 as novel therapeutic agents.


2014 ◽  
Vol 211 (13) ◽  
pp. 2635-2649 ◽  
Author(s):  
Di Wang ◽  
Mingzhu Zheng ◽  
Yuanjun Qiu ◽  
Chuansheng Guo ◽  
Jian Ji ◽  
...  

Antigen-mediated cross-linking of IgE on mast cells triggers a signaling cascade that results in their degranulation and proinflammatory cytokine production, which are key effectors in allergic reactions. We show that the activation of mast cells is negatively regulated by the newly identified adaptor protein Tespa1. Loss of Tespa1 in mouse mast cells led to hyper-responsiveness to stimulation via FcεRI. Mice lacking Tespa1 also displayed increased sensitivity to IgE-mediated allergic responses. The dysregulated signaling in KO mast cells was associated with increased activation of Grb2-PLC-γ1-SLP-76 signaling within the LAT1 (linker for activation of T cells family, member 1) signalosome versus the LAT2 signalosome. Collectively, these findings show that Tespa1 orchestrates mast cell activation by tuning the balance of LAT1 and LAT2 signalosome assembly.


1987 ◽  
Vol 1 (1) ◽  
pp. 17-26 ◽  
Author(s):  
Kenneth P. Mathews

Besides histamine, a large and increasing number of mediators of allergic reactions are being found to be released by mast cells or basophils during anaphylactic reactions. Many of these same substances are released by stimuli other than allergen-IgE interactions, and this type of phenomenon (anaphylactoid or pseudo-allergic reaction) may account for some nasal symptoms that simulate allergy. In addition to rapidly developing reactions of these types, numerous recent investigations have emphasized the importance of late-phase reactions that occur as a consequence of the immediate reactivity. Besides mast cells and/or basophils, these late effects seem to involve a complex network of cellular interactions, which may include neutrophils, eosinophils, lymphocytes, macrophages, and platelets. Studies of nasal washings following allergen challenges in humans have provided cogent in vivo support of earlier hypotheses about mediator release based on in vitro experimentation.


2021 ◽  
Vol 19 (1) ◽  
Author(s):  
Itsuro Kazama

AbstractTo fight against coronavirus disease 2019 (COVID-19), the vaccination is currently the most effective approach. However, in addition to common systemic side effects, the vaccines can cause serious allergic reactions or anaphylaxis. In anaphylaxis, the exposure to the allergen causes a sudden release of chemical mediators from mast cells, for which adrenaline is the drug of first choice. In our previous basic studies, in addition to adrenaline, anti-allergic drugs (olopatadine, loratadine, tranilast and ketotifen), antibiotics (clarithromycin), corticosteroids (hydrocortisone and dexamethasone) and certain food constituents (caffeine and catechin) inhibited the process of exocytosis and showed their effectiveness as highly potent mast cell stabilizers. In these studies, since mast cells were pre-incubated with these drugs or the food constituents before exocytosis was induced, the findings strongly indicated their prophylactic efficacy in stabilizing mast cells. Considering such pharmacological properties of these commonly prescribed medications or the food constituents, their prophylactic use may potentially be beneficial in preventing anaphylaxis caused by COVID-19 vaccination.


Author(s):  
Tatsuki R. Kataoka ◽  
Chiyuki Ueshima ◽  
Masahiro Hirata ◽  
Sachiko Minamiguchi ◽  
Hironori Haga

Killer immunoglobulin-like receptor (KIR) 2DL4 (CD158d) was previously thought to be a human NK-cell-specific protein but its expression has also been demonstrated in human mast cells. Mast cells are involved in allergic reactions via their KIT-mediated and IgE receptor-mediated responses. We recently detected the expression of KIR2DL4 in human cultured mast cells established from peripheral blood derived from healthy volunteers (PB-mast), a human mast cell line (LAD2), and non-neoplastic mast cells, including pathological specimens. An agonistic antibody against KIR2DL4 negatively regulates the KIT- and IgE-receptor-mediated responses of PB-mast and LAD2 cells. In addition, agonistic antibodies and human leukocyte antigen (HLA)-G, a natural ligand for KIR2DL4, induce the secretion from these cells of leukemia inhibitory factor and serine proteases, which have been implicated in pregnancy establishment and cancer metastasis. Therefore, KIR2DL4 stimulation with agonistic antibodies and recombinant HLA-G protein may enhance both processes, in addition to suppressing mast-cell-mediated allergic reactions.


Sign in / Sign up

Export Citation Format

Share Document