Inhibitory Effect of Adenosine on Degranulation of Human Cultured Mast Cells upon Cross-linking of FcϵRI

1998 ◽  
Vol 242 (3) ◽  
pp. 697-702 ◽  
Author(s):  
Hidefumi Suzuki ◽  
Masao Takei ◽  
Tatsutoshi Nakahata ◽  
Hiromi Fukamachi
Keyword(s):  
Mast Cells ◽  
Inhibitory Effect ◽  
Cross Linking

scholarly journals Inhibitory Effect of Crude-Drug Extracts on the Degranulation of Mast Cells (RBL-2H3)

2011 ◽  
Vol 58 (7) ◽  
pp. 330-334 ◽  
Author(s):  
Mariko Asano ◽  
Megumi Dohi ◽  
Kazunaga Yazawa ◽  
Takashi Kometani ◽  
Kyoko Takahashi
Keyword(s):  
Mast Cells ◽  
Inhibitory Effect ◽  
Crude Drug

Analysis of mouse LMIR5/CLM-7 as an activating receptor: differential regulation of LMIR5/CLM-7 in mouse versus human cells

Blood ◽  
2008 ◽  
Vol 111 (2) ◽  
pp. 688-698 ◽  
Author(s):  
Yoshinori Yamanishi ◽  
Jiro Kitaura ◽  
Kumi Izawa ◽  
Takayuki Matsuoka ◽  
Toshihiko Oki ◽  
...  
Keyword(s):  
Mast Cells ◽  
Cytokine Production ◽  
Fetal Liver ◽  
Human Cells ◽  
Cross Linking ◽  
Wild Type ◽  
Predominant Role ◽  
Innate Immunity Cells ◽  
Production Cell ◽  
Activating Receptor

We have analyzed leukocyte mono-Ig–like receptor 5 (LMIR5) as an activating receptor among paired LMIRs. Mouse LMIR5 (mLMIR5) is expressed in myeloid cells such as mast cells, granulocytes, macrophages, and dendritic cells. Cross-linking of transduced mLMIR5 in bone marrow–derived mast cells (BMMCs) caused activation events, including cytokine production, cell survival, degranulation, and adhesion to the extracellular matrix. mLMIR5 associated with DAP12 and to a lesser extent with DAP10, and mLMIR5-mediated functions of BMMCs were strongly inhibited by DAP12 deficiency. Importantly, cross-linking of endogenous mLMIR5 induced Syk-dependent activation of fetal liver–derived mast cells. Unlike mLMIR5, cross-linking of human LMIR5 (hLMIR5) induced cytokine production of BMMCs even in the absence of both DAP12 and DAP10, suggesting the existence of unidentified adaptors. Interestingly, hLMIR5 possessed a tyrosine residue (Y188) in the cytoplasmic region. Signaling via Y188 phosphorylation played a predominant role in hLMIR5-mediated cytokine production in DAP12-deficient, but not wild-type BMMCs. In addition, experiments using DAP10/DAP12 double-deficient BMMCs suggested the existence of Y188 phoshorylation-dependent and -independent signals from unidentified adaptors. Collectively, although both mouse and human LMIR5 play activatory roles in innate immunity cells, the functions of LMIR5 were differentially regulated in mouse versus human cells.

Impact of mast cells in depression disorder: inhibitory effect of IL-37 (new frontiers)

2018 ◽  
Vol 66 (3) ◽  
pp. 323-331 ◽  
Author(s):  
Pio Conti ◽  
Alessandro Caraffa ◽  
Gianpaolo Ronconi ◽  
Chiara M. Conti ◽  
Spiros K. Kritas ◽  
...  
Keyword(s):  
Mast Cells ◽  
Inhibitory Effect ◽  
Depression Disorder

scholarly journals The emerging role of mast cell proteases in asthma

2019 ◽  
Vol 54 (4) ◽  
pp. 1900685 ◽  
Author(s):  
Gunnar Pejler
Keyword(s):  
Mast Cell ◽  
Mast Cells ◽  
Current Knowledge ◽  
Secretory Granules ◽  
Cross Linking ◽  
Lysosomal Hydrolases ◽  
Ige Receptor ◽  
Deficient Mice ◽  
Lines Of Evidence

It is now well established that mast cells (MCs) play a crucial role in asthma. This is supported by multiple lines of evidence, including both clinical studies and studies on MC-deficient mice. However, there is still only limited knowledge of the exact effector mechanism(s) by which MCs influence asthma pathology. MCs contain large amounts of secretory granules, which are filled with a variety of bioactive compounds including histamine, cytokines, lysosomal hydrolases, serglycin proteoglycans and a number of MC-restricted proteases. When MCs are activated, e.g. in response to IgE receptor cross-linking, the contents of their granules are released to the exterior and can cause a massive inflammatory reaction. The MC-restricted proteases include tryptases, chymases and carboxypeptidase A3, and these are expressed and stored at remarkably high levels. There is now emerging evidence supporting a prominent role of these enzymes in the pathology of asthma. Interestingly, however, the role of the MC-restricted proteases is multifaceted, encompassing both protective and detrimental activities. Here, the current knowledge of how the MC-restricted proteases impact on asthma is reviewed.

Inhibitory Effect of Retinoic Acid on Proliferation, Maturation and Tryptase Level in Human Leukemic Mast Cells (HMC-1)

2003 ◽  
Vol 16 (1) ◽  
pp. 43-47 ◽  
Author(s):  
M.G. Alexandrakis ◽  
D.S. Kyriakou ◽  
D. Seretakis ◽  
W. Boucher ◽  
R. Letourneau ◽  
...  
Keyword(s):  
Mast Cell ◽  
Retinoic Acid ◽  
Mast Cells ◽  
Allergic Inflammation ◽  
Inhibitory Effect ◽  
Control Group ◽  
Tryptase Level ◽  
Synthetic Derivatives ◽  
Derivatives Of ◽  
Inhibit Cell Proliferation

Mast cells play an important role in allergic inflammation by releasing histamine, tryptase and several inflammatory cytokines. Human leukemic mast cells (HMC-1) have been used to study mast cell mediators and their role in inflammatory mechanisms. HMC-1 contain and release several inflammatory mediators, of which the proteolytic enzyme tryptase is most characteristic. Retinoids, including retinoic acid, are naturally occurring and synthetic derivatives of vitamin A. All-trans-retinoic (ATRA) acid had been previously reported to inhibit cell proliferation, differentiation and apoptosis. In the present study, we investigated the effect of ATRA on the proliferation and secretion of tryptase in HMC-1. HMC-1 were treated with ATRA at 10-4M, 10-5M or 10-6M for 3,4 or 5 days in culture. Control HMC-1 were treated with equal amount of culture medium only. ATRA decreased the number of HMC-1 as compared to the control group. The same treatment for 3, 4 or 5 days also decreased intracellular tryptase levels. These results indicate that ATRA significantly inhibits both proliferation and growth as shown by the decreased intracellular tryptase levels in HMC-1. ATRA may be a useful agent in the treatment of mast cell proliferative disorders.

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