PLoS biology, 2014-01, Vol.12 (1), p.e1001762
2014
Details
- Autor(en) / Beteiligte
- Titel
- A20-deficient mast cells exacerbate inflammatory responses in vivo
- Ist Teil von
- PLoS biology, 2014-01, Vol.12 (1), p.e1001762
- Ort / Verlag
- United States: Public Library of Science
- Erscheinungsjahr
- 2014
- Link zum Volltext
- Quelle
- MEDLINE
- Beschreibungen/Notizen
- Mast cells are implicated in the pathogenesis of inflammatory and autoimmune diseases. However, this notion based on studies in mast cell-deficient mice is controversial. We therefore established an in vivo model for hyperactive mast cells by specifically ablating the NF-κB negative feedback regulator A20. While A20 deficiency did not affect mast cell degranulation, it resulted in amplified pro-inflammatory responses downstream of IgE/FcεRI, TLRs, IL-1R, and IL-33R. As a consequence house dust mite- and IL-33-driven lung inflammation, late phase cutaneous anaphylaxis, and collagen-induced arthritis were aggravated, in contrast to experimental autoimmune encephalomyelitis and immediate anaphylaxis. Our results provide in vivo evidence that hyperactive mast cells can exacerbate inflammatory disorders and define diseases that might benefit from therapeutic intervention with mast cell function.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1545-7885, 1544-9173eISSN: 1545-7885DOI: 10.1371/journal.pbio.1001762Titel-ID: cdi_plos_journals_1498391802
- Format
- –
- Schlagworte
- Allergies, Anaphylaxis - chemically induced, Anaphylaxis - immunology, Anaphylaxis - metabolism, Anaphylaxis - pathology, Animals, Antigens, Arthritis, Arthritis, Experimental - chemically induced, Arthritis, Experimental - immunology, Arthritis, Experimental - metabolism, Arthritis, Experimental - pathology, Asthma, Biology, Collagen Type II - administration & dosage, Cysteine Endopeptidases, Cytokines, Dinitrophenols - administration & dosage, Disease, DNA-Binding Proteins - deficiency, DNA-Binding Proteins - genetics, DNA-Binding Proteins - immunology, Encephalomyelitis, Autoimmune, Experimental - chemically induced, Encephalomyelitis, Autoimmune, Experimental - immunology, Encephalomyelitis, Autoimmune, Experimental - metabolism, Encephalomyelitis, Autoimmune, Experimental - pathology, Experiments, Gene Expression, Grants, Histamine, Immunoglobulin E - genetics, Immunoglobulin E - immunology, Interleukin-1 Receptor-Like 1 Protein, Interleukin-33, Interleukins - genetics, Interleukins - immunology, Intracellular Signaling Peptides and Proteins - deficiency, Intracellular Signaling Peptides and Proteins - genetics, Intracellular Signaling Peptides and Proteins - immunology, Kinases, Lung - immunology, Lung - metabolism, Lung - pathology, Male, Mast Cells - immunology, Mast Cells - metabolism, Mast Cells - pathology, Mice, Mice, Transgenic, Myelin-Oligodendrocyte Glycoprotein - administration & dosage, NF-kappa B - genetics, NF-kappa B - immunology, Pattern recognition, Peptide Fragments - administration & dosage, Pneumonia - chemically induced, Pneumonia - immunology, Pneumonia - metabolism, Pneumonia - pathology, Pyroglyphidae - immunology, Receptors, IgE - genetics, Receptors, IgE - immunology, Receptors, Interleukin - genetics, Receptors, Interleukin - immunology, Receptors, Interleukin-1 - genetics, Receptors, Interleukin-1 - immunology, Rodents, Serum Albumin, Bovine - administration & dosage, Studies, Toll-Like Receptors - genetics, Toll-Like Receptors - immunology, Tumor Necrosis Factor alpha-Induced Protein 3, Ubiquitin-Protein Ligases - deficiency, Ubiquitin-Protein Ligases - genetics, Ubiquitin-Protein Ligases - immunology