Stem cell factor programs the mast cell activation phenotype
Mast cells, activated by Ag via FcεRI, release an array of proinflammatory mediators that contribute to allergic disorders, such as asthma and anaphylaxis. The KIT ligand, stem cell factor (SCF), is critical for mast cell expansion, differentiation, and survival, and under acute conditions, it enhan...
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| Published in | The Journal of immunology (1950) Vol. 188; no. 11; pp. 5428 - 5437 |
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| Main Authors | , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
01.06.2012
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| Subjects | |
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| Abstract | Mast cells, activated by Ag via FcεRI, release an array of proinflammatory mediators that contribute to allergic disorders, such as asthma and anaphylaxis. The KIT ligand, stem cell factor (SCF), is critical for mast cell expansion, differentiation, and survival, and under acute conditions, it enhances mast cell activation. However, extended SCF exposure in vivo conversely protects against fatal Ag-mediated anaphylaxis. In investigating this dichotomy, we identified a novel mode of regulation of the mast cell activation phenotype through SCF-mediated programming. We found that mouse bone marrow-derived mast cells chronically exposed to SCF displayed a marked attenuation of FcεRI-mediated degranulation and cytokine production. The hyporesponsive phenotype was not a consequence of altered signals regulating calcium flux or protein kinase C, but of ineffective cytoskeletal reorganization with evidence implicating a downregulation of expression of the Src kinase Hck. Collectively, these findings demonstrate a major role for SCF in the homeostatic control of mast cell activation with potential relevance to mast cell-driven disease and the development of novel approaches for the treatment of allergic disorders. |
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| AbstractList | Mast cells, activated by Ag via Fc epsilon RI, release an array of proinflammatory mediators that contribute to allergic disorders, such as asthma and anaphylaxis. The KIT ligand, stem cell factor (SCF), is critical for mast cell expansion, differentiation, and survival, and under acute conditions, it enhances mast cell activation. However, extended SCF exposure in vivo conversely protects against fatal Ag-mediated anaphylaxis. In investigating this dichotomy, we identified a novel mode of regulation of the mast cell activation phenotype through SCF-mediated programming. We found that mouse bone marrow-derived mast cells chronically exposed to SCF displayed a marked attenuation of Fc epsilon RI-mediated degranulation and cytokine production. The hyporesponsive phenotype was not a consequence of altered signals regulating calcium flux or protein kinase C, but of ineffective cytoskeletal reorganization with evidence implicating a downregulation of expression of the Src kinase Hck. Collectively, these findings demonstrate a major role for SCF in the homeostatic control of mast cell activation with potential relevance to mast cell-driven disease and the development of novel approaches for the treatment of allergic disorders. Mast cells, activated by Ag via FcεRI, release an array of proinflammatory mediators that contribute to allergic disorders, such as asthma and anaphylaxis. The KIT ligand, stem cell factor (SCF), is critical for mast cell expansion, differentiation, and survival, and under acute conditions, it enhances mast cell activation. However, extended SCF exposure in vivo conversely protects against fatal Ag-mediated anaphylaxis. In investigating this dichotomy, we identified a novel mode of regulation of the mast cell activation phenotype through SCF-mediated programming. We found that mouse bone marrow-derived mast cells chronically exposed to SCF displayed a marked attenuation of FcεRI-mediated degranulation and cytokine production. The hyporesponsive phenotype was not a consequence of altered signals regulating calcium flux or protein kinase C, but of ineffective cytoskeletal reorganization with evidence implicating a downregulation of expression of the Src kinase Hck. Collectively, these findings demonstrate a major role for SCF in the homeostatic control of mast cell activation with potential relevance to mast cell-driven disease and the development of novel approaches for the treatment of allergic disorders. Mast cells, activated by antigen via the high affinity receptor for IgE (FcεRI), release an array of pro-inflammatory mediators that contribute to allergic disorders such as asthma and anaphylaxis. The KIT ligand, stem cell factor (SCF), is critical for mast cell expansion, differentiation and survival, and, under acute conditions, enhances mast cell activation. However, extended SCF exposure in vivo conversely protects against fatal antigen-mediated anaphylaxis. In investigating this dichotomy, we identified a novel mode of regulation of the mast cell activation phenotype through SCF-mediated programming. We found that mouse bone marrow-derived mast cells chronically exposed to SCF displayed a marked attenuation of FcεRI-mediated degranulation and cytokine production. The hypo-responsive phenotype was not a consequence of altered signals regulating calcium flux or protein kinase C, but of ineffective cytoskeletal reorganization, with evidence implicating a down-regulation of expression of the Src kinase Hck. Collectively, these findings demonstrate a major role for SCF in the homeostatic control of mast cell activation with potential relevance to mast cell-driven disease and the development of novel approaches for the treatment of allergic disorders. |
| Author | Ito, Tomonobu Smrž, Daniel Beaven, Michael A Bandara, Geethani Kuehn, Hye Sun Gilfillan, Alasdair M Metcalfe, Dean D Desai, Avanti Smržová, Šárka Jung, Mi-Yeon |
| AuthorAffiliation | Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive MSC 1881, Bethesda, MD 20892-1881, USA Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA |
| AuthorAffiliation_xml | – name: Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, 10 Center Drive MSC 1881, Bethesda, MD 20892-1881, USA – name: Laboratory of Molecular Immunology, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA |
| Author_xml | – sequence: 1 givenname: Tomonobu surname: Ito fullname: Ito, Tomonobu organization: Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA – sequence: 2 givenname: Daniel surname: Smrž fullname: Smrž, Daniel – sequence: 3 givenname: Mi-Yeon surname: Jung fullname: Jung, Mi-Yeon – sequence: 4 givenname: Geethani surname: Bandara fullname: Bandara, Geethani – sequence: 5 givenname: Avanti surname: Desai fullname: Desai, Avanti – sequence: 6 givenname: Šárka surname: Smržová fullname: Smržová, Šárka – sequence: 7 givenname: Hye Sun surname: Kuehn fullname: Kuehn, Hye Sun – sequence: 8 givenname: Michael A surname: Beaven fullname: Beaven, Michael A – sequence: 9 givenname: Dean D surname: Metcalfe fullname: Metcalfe, Dean D – sequence: 10 givenname: Alasdair M surname: Gilfillan fullname: Gilfillan, Alasdair M |
| BackLink | https://www.ncbi.nlm.nih.gov/pubmed/22529299$$D View this record in MEDLINE/PubMed |
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| SubjectTerms | Animals Bone Marrow Cells - cytology Bone Marrow Cells - immunology Bone Marrow Cells - metabolism Cell Degranulation - immunology Cell Proliferation Cells, Cultured Coculture Techniques Homeostasis - immunology Hypersensitivity - immunology Hypersensitivity - metabolism Hypersensitivity - pathology Immunophenotyping Mast Cells - cytology Mast Cells - immunology Mast Cells - metabolism Mice Mice, Inbred C57BL NIH 3T3 Cells Stem Cell Factor - physiology |
| Title | Stem cell factor programs the mast cell activation phenotype |
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