Mast Cell Studies
distributions~gut and air tract, joints,choroid (眼脉络膜），liver, artery,
cytokines derived~ proinflammatory, allergic response, degradation of tissue,
`histamine, trypatse, heparin, leukotrienes, prostaglandins, chondrontin sulfate, aryl sulfatase, also IL-10
tryptase，protease from mast cells
Mast Cell Biology
Mast cells are tissue resident, granule-containing cells capable of regulating both the innate and adaptive immune response (26). Enrichment of mast cells at environmental interfaces allows these cells to be among the first to respond during pathogen invasion, along with dendritic cells and epithelial cells (27). Moreover, mast cells are typically situated near blood vessels, lymphatics, and nerve endings, enabling them to have long range effects on the host response to pathogens (27, 28). As such, mast cells are critical to immune surveillance, eliciting an immediate reaction to invading pathogens and initiating an appropriate innate and adaptive immune response.
The lung is protected from pathogens by alveolar epithelial cells, endothelial cells, tissue resident alveolar macrophages, dendritic cells, and mast cells.
Figure 1. Mast cell activation in response to viral infection. Mast cells are classically known for their response to polyvalent cross-linking of IgE in the FcϵR1 receptor, which is important in protective immunity to helminth worm infection and pathologically associated with allergic disease. However, mast cells also are important tissue sentinel cells for initiating inflammatory response to pathogens. Mast cells can recognize and respond to viruses through several different receptors. These receptors include TLR signaling, such as TLR3 detection of dsRNA, sphingosin-1-phosphate (S1P) binding to its receptor S1PR, and RIG-I recognition of uncapped vRNA. Engagement of these receptors results in mast cell activation leading to immediate degranulation, the de novo synthesis of eicosanoids within minutes of activation, and the de novo synthesis of numerous cytokines, chemokines, and growth factors within hours of activation.
Frontiers | Mast Cell: A Multi-Functional Master Cell | Immunology (frontiersin.org)
Mast Cells Respond to Cell Injury through the Recognition of IL-33
IL-33 is a member of a big IL-1 cytokine family that regulates innate and adaptive immune systems to promote inflammatory responses . In contrast to the action of IL-1, which is processed and released by live immune cells in response to infection or other triggers, IL-33 acts as an alarmin against injury-induced stress, pathogens, or cell death by activating local immune cells [21,22]. IL-33 is a cytokine with dualfunction. ...
IL-33 is a cytokine that is constitutively expressed in the nuclei of endothelial and epithelial cells [10,11]. The full-length of IL-33, pro-IL-33, serves as a gene regulator that is localized in the nuclei , whereas mature IL-33 serves as a cytokine after release into the extracellular space at the onset of tissue injury [13,14]. C-reactive protein (CRP) is an acute-phase protein that serves as an early marker of inflammation or infection. ...
... IL-4, on the other hand, is the signature cytokine of type-2 immunity, IgE-mediated hypersensitivity and can increase proliferation and several MC attributes  . IL-33 acts as an "alarmin" released from damaged or injured cells, initiating inflammation, but also Th2-skewed immunity; one of its major target cells is the MC, on which it exerts potent phenotypical and functional effects [26,27] . Finally, retinoic acid (RA) has a crucial function in the skin (both as endogenous hormone and therapeutically), and it is skin MCs that are highly enriched with components of the retinoid network vis-à-vis all major skin cells; consequently skin MCs are potently reshaped by RA  . ...
Mast cells respond to IL-33 released during cell injury by initiating a... | Download Scientific Diagram
Mast cells (MCs) are the principal effector cells of IgE-mediated allergy. IL-33 is released by resident skin cells as alarmin upon tissue damage or allergen contact. Owing to their pronounced receptor expression, MCs are important targets of IL-33 action, but consequences for skin MCs are ill-defined, especially upon chronic exposure to IL-33. Mimicking the inflammatory milieu of skin disorders, we found that persistent exposure to IL-33 (over a 5-week period) strengthened skin MC numbers through accelerated cell-cycle progression and restriction of apoptosis. Conversely, IL-33 attenuated degranulation and FcεRI expression, potentially as a feedback to chronic “alarmin” exposure. Interestingly, the negative impact on histamine release was counterbalanced by amplified histamine production. Considering the clinical significance of histamine and scarce information on its regulation, we explored the molecular underpinnings. IL-33 induced swift phosphorylation of p38 and JNK (but not of ERK1/2 or AKT), and stimulated histidine decarboxylase expression. Combining pharmacological inhibition and kinase elimination by Accell-facilitated RNA interference in skin MCs revealed a p38-dependent, but JNK-independent mechanism. Collectively, IL-33 exerts multifaceted effects on cutaneous MCs at a post-maturation stage. The IL-33–skin MC axis may contribute to and balance inflammation in chronic skin disorders.
Yin-Yang of IL-33 in Human Skin Mast Cells: Reduced Degranulation, but Augmented Histamine Synthesis through p38 Activation | Request PDF
Effects of essential fatty acids on mediators of mast cells in culture
The objective of this study was to investigate the effects of α-linolenic acid (18:3n-3) and linoleic acid (18:2n-6) on the fatty acid composition and the activity and release of mast cell mediators in the canine mastocytoma cell line C2. Cells were cultured in Dulbecco's modified Eagle's medium mixed with 50% Ham's F12 (containing linoleic acid 0.14 μM). The basic medium (DEH) was supplemented with 0.14 μM α-linolenic acid. 14.0 μM α-linolenic acid (DEH-n-3) or 14.0 μM linoleic acid (DEH-n-6) was added. Eight days after culturing of C2 in DEH-n-3 we measured elevated levels of n-3 fatty acids up to 22:3. The tryptase activity and the stimulated PGE2 production and histamine release were reduced. In contrast, after culturing of C2 in DEH-n-6 we determined elevated levels of n-6 fatty acids up to 20:3, increased tryptase activity and stimulated histamine release. Thus 18:3n-3 has anti-inflammatory effects in cultured canine mastocytoma cells.
这项研究的目的是研究α-亚麻酸（18：3n-3）和亚油酸（18：2n-6）对犬肥大细胞瘤细胞系C2中脂肪酸组成以及肥大细胞介质的活性和释放的影响。将细胞在与50％Ham's F12（含0.14μM亚油酸）混合的Dulbecco's改良Eagle培养基中培养。基本培养基（DEH）补充有0.14μM α-亚麻酸。添加14.0μ M的α-亚麻酸（DEH-n-3）或14.0μM的亚油酸（DEH-n-6）。在DEH-n-3中培养C2八天后，我们测量到高达22：3的n-3脂肪酸水平升高。降低了类胰蛋白酶的活性以及刺激的PGE2的产生和组胺的释放。相反，在DEH-n-6中培养C2后，我们确定了高达20：3的n-6脂肪酸水平升高，类胰蛋白酶活性增加和组胺释放受到刺激。因此，18：3n-3在培养的犬肥大细胞瘤细胞中具有抗炎作用。
Effects of essential fatty acids on mediators of mast cells in culture - ScienceDirect
Mast Cell Interleukin-10 Drives Localized Tolerance in ...
Mast Cell Interleukin-10 Drives Localized Tolerance in Chronic Bladder Infection. Previous Article Human Inflammatory Dendritic Cells Induce Th17 Cell Differentiation. Next Article Interleukin-9 Is Required for Allergic Airway Inflammation Mediated by the Cytokine TSLP. Summary.
Cited by: 140
Publish Year: 2013
Author: Cheryl Y. Chan, Ashley L. St. John, Soman N. Abraham
Induction of Interleukin-10 Producing Dendritic Cells As a ...
Mar 19, 2018 · Among the cytokines produced by tolerogenic DCs, interleukin 10 (IL-10) is a key regulatory cytokine limiting und ultimately terminating excessive T-cell responses to microbial pathogens to prevent chronic inflammation and tissue damage.