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  • 1
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    The development of allergic inflammation (2008)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2008-07-25
    Description: Allergic disorders, such as anaphylaxis, hay fever, eczema and asthma, now afflict roughly 25% of people in the developed world. In allergic subjects, persistent or repetitive exposure to allergens, which typically are intrinsically innocuous substances common in the environment, results in chronic allergic inflammation. This in turn produces long-term changes in the structure of the affected organs and substantial abnormalities in their function. It is therefore important to understand the characteristics and consequences of acute and chronic allergic inflammation, and in particular to explore how mast cells can contribute to several features of this maladaptive pattern of immunological reactivity.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3573758/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3573758/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galli, Stephen J -- Tsai, Mindy -- Piliponsky, Adrian M -- R01 AI023990/AI/NIAID NIH HHS/ -- R01 AI023990-20/AI/NIAID NIH HHS/ -- R01 AI070813/AI/NIAID NIH HHS/ -- R01 AI070813-01/AI/NIAID NIH HHS/ -- R01 CA072074/CA/NCI NIH HHS/ -- R01 CA072074-15/CA/NCI NIH HHS/ -- England -- Nature. 2008 Jul 24;454(7203):445-54. doi: 10.1038/nature07204.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University School of Medicine, 300 Pasteur Drive, Stanford, California 94305, USA. sgalli@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/18650915" target="_blank"〉PubMed〈/a〉
    Keywords: Allergens/immunology ; Animals ; Chronic Disease ; Epithelium/immunology ; Humans ; Hypersensitivity/genetics/*immunology/*pathology ; Immunoglobulin E/immunology ; Inflammation/genetics/*immunology/*pathology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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  • 2
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    Mast cells can enhance resistance to snake and honeybee venoms (2006)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2006-07-29
    Description: Snake or honeybee envenomation can cause substantial morbidity and mortality, and it has been proposed that the activation of mast cells by snake or insect venoms can contribute to these effects. We show, in contrast, that mast cells can significantly reduce snake-venom-induced pathology in mice, at least in part by releasing carboxypeptidase A and possibly other proteases, which can degrade venom components. Mast cells also significantly reduced the morbidity and mortality induced by honeybee venom. These findings identify a new biological function for mast cells in enhancing resistance to the morbidity and mortality induced by animal venoms.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Metz, Martin -- Piliponsky, Adrian M -- Chen, Ching-Cheng -- Lammel, Verena -- Abrink, Magnus -- Pejler, Gunnar -- Tsai, Mindy -- Galli, Stephen J -- P50 HL067674/HL/NHLBI NIH HHS/ -- P50 HL67674/HL/NHLBI NIH HHS/ -- R01 AI023990/AI/NIAID NIH HHS/ -- R01 CA072074/CA/NCI NIH HHS/ -- R01 CA72074/CA/NCI NIH HHS/ -- R37 AI23990/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2006 Jul 28;313(5786):526-30.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Stanford University School of Medicine, Stanford, CA 94305-5324, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/16873664" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Bee Venoms/*antagonists & inhibitors/toxicity ; Carboxypeptidases A/antagonists & inhibitors/*metabolism ; Cell Degranulation ; Chymases ; Crotalid Venoms/*antagonists & inhibitors/metabolism/toxicity ; Hypothermia/etiology ; Immunity, Innate ; Mast Cells/enzymology/immunology/*physiology ; Mice ; Mice, Inbred C57BL ; Peptide Hydrolases/metabolism ; Peritoneal Cavity/cytology ; Plant Proteins/pharmacology ; Protease Inhibitors ; Serine Endopeptidases/metabolism ; Viper Venoms/*antagonists & inhibitors/metabolism/toxicity
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 3
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    Identification of a committed precursor for the mast cell lineage (1996)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1996-02-09
    Description: Mast cells originate from hematopoietic stem cells, but the mast cell-committed precursor has not been identified. In the study presented here, a cell population in murine fetal blood that fulfills the criteria of progenitor mastocytes was identified. It is defined by the phenotype Thy-1loc-Kithi, contains cytoplasmic granules, and expresses RNAs encoding mast cell-associated proteases but lacks expression of the high-affinity immunoglobulin E receptor. Thy-1loc-Kithi cells generated functionally competent mast cells at high frequencies in vitro but lacked developmental potential for other hematopoietic lineages. When transferred intraperitoneally, this population reconstituted the peritoneal mast cell compartment of genetically mast cell-deficient W/Wv mice to wild-type levels.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rodewald, H R -- Dessing, M -- Dvorak, A M -- Galli, S J -- AI-33372/AI/NIAID NIH HHS/ -- AI/CA-23990/AI/NIAID NIH HHS/ -- CA/AI-72074/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 1996 Feb 9;271(5250):818-22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Basel Institute for Immunology, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/8629001" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Thy-1/analysis ; Base Sequence ; Cell Lineage ; Cell Transplantation ; Cells, Cultured ; Cytoplasmic Granules/ultrastructure ; Endopeptidases/genetics/metabolism ; Fetal Blood ; Hematopoietic Stem Cells/*cytology/physiology/ultrastructure ; Immunophenotyping ; Interleukin-3/pharmacology ; Mast Cells/*cytology/physiology/ultrastructure ; Mice ; Molecular Sequence Data ; Peritoneal Cavity/cytology ; Proto-Oncogene Proteins c-kit/analysis ; RNA, Messenger/genetics/metabolism ; Receptors, IgE/analysis/genetics ; Stem Cell Factor/pharmacology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 4
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    Unequivocal delayed hypersensitivity in mast cell-deficient and beige mice (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-11-09
    Description: It has been suggested that reserpine blocks expression of delayed hypersensitivity in mice because it depletes stores of the vasoactive amine serotonin in mast cells. To determine whether mast cell serotonin or other mast cell-derived mediators are essential for delayed hypersensitivity, responses to contact sensitizers in mast cell-deficient W/Wv or Sl/Sld mice were studied. Because blood platelets represent another potential source of serotonin in delayed hypersensitivity responses, beige mice, whose platelets contain less than 1 percent of the normal levels of serotonin, were also examined. By the criteria of tissue swelling, infiltration of iodinated leukocytes, or histology, mast cell-deficient or beige mice expressed delayed hypersensitivity reactions whose intensity generally equaled or exceeded that of reactions in littermate controls. In addition, reserpine blocked delayed hypersensitivity in W/Wv and beige mice, suggesting that effects on mast cell or platelet serotonin cannot explain this drug's action in delayed hypersensitivity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galli, S J -- Hammel, I -- AI 20292/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 1984 Nov 9;226(4675):710-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6494907" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Drug Hypersensitivity/etiology ; Humans ; Hypersensitivity, Delayed/*physiopathology ; Mast Cells/*physiology ; Methysergide/pharmacology ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains/immunology ; Oxazolone/pharmacology ; Reserpine/pharmacology ; Serotonin/physiology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 5
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    Uncertainty of histologic classification of experimental tumors (1984)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1984-10-19
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Galli, S J -- New York, N.Y. -- Science. 1984 Oct 19;226(4672):352-3.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6484574" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Neoplasms, Experimental/classification/*pathology ; Rats
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 6
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    Tumor cells secrete a vascular permeability factor that promotes accumulation of ascites fluid (1983)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 1983-02-25
    Description: Tumor ascites fluids from guinea pigs, hamsters, and mice contain activity that rapidly increases microvascular permeability. Similar activity is also secreted by these tumor cells and a variety of other tumor cell lines in vitro. The permeability-increasing activity purified from either the culture medium or ascites fluid of one tumor, the guinea pig line 10 hepatocarcinoma, is a 34,000- to 42,000-dalton protein distinct from other known permeability factors.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Senger, D R -- Galli, S J -- Dvorak, A M -- Perruzzi, C A -- Harvey, V S -- Dvorak, H F -- New York, N.Y. -- Science. 1983 Feb 25;219(4587):983-5.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/6823562" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ascites/physiopathology ; Ascitic Fluid/physiology ; *Capillary Permeability ; Cricetinae ; Guinea Pigs ; Mice ; Neoplasms, Experimental/*physiopathology
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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  • 7
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    MIBI-TOF: A multiplexed imaging platform relates cellular phenotypes and tissue structure (2019)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2019
    Description: 〈p〉Understanding tissue structure and function requires tools that quantify the expression of multiple proteins while preserving spatial information. Here, we describe MIBI-TOF (multiplexed ion beam imaging by time of flight), an instrument that uses bright ion sources and orthogonal time-of-flight mass spectrometry to image metal-tagged antibodies at subcellular resolution in clinical tissue sections. We demonstrate quantitative, full periodic table coverage across a five-log dynamic range, imaging 36 labeled antibodies simultaneously with histochemical stains and endogenous elements. We image fields of view up to 800 μm x 800 μm at resolutions down to 260 nm with sensitivities approaching single-molecule detection. We leverage these properties to interrogate intrapatient heterogeneity in tumor organization in triple-negative breast cancer, revealing regional variability in tumor cell phenotypes in contrast to a structured immune response. Given its versatility and sample back-compatibility, MIBI-TOF is positioned to leverage existing annotated, archival tissue cohorts to explore emerging questions in cancer, immunology, and neurobiology.〈/p〉
    Electronic ISSN: 2375-2548
    Topics: Natural Sciences in General
    Published by American Association for the Advancement of Science (AAAS)
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  • 8
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    Multiple elements of the allergic arm of the immune response modulate autoimmune demyelination (2003)
    National Academy of Sciences
    Details
    Publication Date: 2003-02-07
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 9
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    Induction of mast cell proliferation, maturation, and heparin synthesis by the rat c-kit ligand, stem cell factor. (1991)
    National Academy of Sciences
    Details
    Publication Date: 1991-07-15
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 10
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    Mast cells are critical for controlling the bacterial burden and the healing of infected wounds (2019)
    National Academy of Sciences
    Details
    Publication Date: 2019-09-23
    Description: Skin wound infections are a significant health problem, and antibiotic resistance is on the rise. Mast cells (MCs) have been shown to contribute to host–defense responses in certain bacterial infections, but their role in skin wound superinfection is unknown. We subjected 2 MC-deficient mouse strains to Pseudomonas aeruginosa skin wound infection and found significantly delayed wound closure in infected skin wounds. This delay was associated with impaired bacterial clearance in the absence of MCs. Engraftment of MCs restored both bacterial clearance and wound closure. Bacterial killing was dependent on IL-6 released from MCs, and engraftment with IL-6–deficient MCs failed to control wound infection. Treatment with recombinant IL-6 enhanced bacterial killing and resulted in the control of wound infection and normal wound healing in vivo. Taken together, our results demonstrate a defense mechanism for boosting host innate immune responses, namely effects of MC-derived IL-6 on antimicrobial functions of keratinocytes.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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