NDLI: IL-33 induces a hyporesponsive phenotype in human and mouse mast cells.

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IL-33 induces a hyporesponsive phenotype in human and mouse mast cells.

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IL-33 induces a hyporesponsive phenotype in human and mouse mast cells.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Iwaki, Shoko Smrz, Daniel Kang, Jeong-Han Metcalfe, Dean D. Ito, Tomonobu Gilfillan, Alasdair M. Brown, Jared M. Bandara, Geethani Hilderbrand, Susana C. Beaven, Michael A. Desai, Avanti Jung, Mi-Yeon Andrade, Marcus V.
Description	Country affiliation: United States Author Affiliation: Jung MY ( Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.)
Abstract	IL-33 is elevated in afflicted tissues of patients with mast cell (MC)-dependent chronic allergic diseases. Based on its acute effects on mouse MCs, IL-33 is thought to play a role in the pathogenesis of allergic disease through MC activation. However, the manifestations of prolonged IL-33 exposure on human MC function, which best reflect the conditions associated with chronic allergic disease, are unknown. In this study, we found that long-term exposure of human and mouse MCs to IL-33 results in a substantial reduction of MC activation in response to Ag. This reduction required >72 h exposure to IL-33 for onset and 1-2 wk for reversion following IL-33 removal. This hyporesponsive phenotype was determined to be a consequence of MyD88-dependent attenuation of signaling processes necessary for MC activation, including Ag-mediated calcium mobilization and cytoskeletal reorganization, potentially as a consequence of downregulation of the expression of phospholipase CÎ³(1) and Hck. These findings suggest that IL-33 may play a protective, rather than a causative, role in MC activation under chronic conditions and, furthermore, reveal regulated plasticity in the MC activation phenotype. The ability to downregulate MC activation in this manner may provide alternative approaches for treatment of MC-driven disease.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1201576
Journal	The Journal of Immunology
Issue Number	2
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-01-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Immunosuppression Interleukins Immunology Mast Cells Metabolism Phenotype Actins Animals Bone Marrow Cells Drug Effects Interleukin-33 Pharmacology Mice Mice, Knockout Myeloid Differentiation Factor 88 Genetics Phospholipase C Gamma Protein Multimerization Proto-oncogene Proteins C-hck Receptors, Interleukin Research Support, N.i.h., Extramural Research Support, N.i.h., Intramural Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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