NDLI: Full-length IL-33 promotes inflammation but not Th2 response in vivo in an ST2-independent fashion.

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Full-length IL-33 promotes inflammation but not Th2 response in vivo in an ST2-independent fashion.

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Full-length IL-33 promotes inflammation but not Th2 response in vivo in an ST2-independent fashion.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Luzina, Irina G. Kopach, Pavel Todd, Nevins W. Kang, Phillip H. Atamas, Sergei P. Lockatell, Virginia McKenzie, Andrew N. J. Papadimitriou, John C. Pickering, Edward M.
Description	Country affiliation: United States Author Affiliation: Luzina IG ( Division of Rheumatology and Clinical Immunology, Department of Medicine, University of Maryland School of Medicine, Baltimore, MD 21201, USA.)
Abstract	Expression of IL-33 is elevated in patients with pulmonary diseases, and full-length (not proteolytically processed) IL-33 is the predominant form in the lungs in health and disease. To determine whether activation of IL-33 is needed for functional effects, activities of full-length mouse and mature mouse (mm) forms of IL-33 were compared in vivo. Replication-deficient adenoviral constructs were used for gene delivery. Both isoforms caused pulmonary infiltration of lymphocytes and neutrophils, whereas mm IL-33 also caused pulmonary eosinophilia and goblet cell hyperplasia and increased expression of IL-4, IL-5, IL-13, IL-17, MCP-1, and KC. The different effects were not associated with differential release from IL-33-producing cells or by differences in subcellular distributions of IL-33 isoforms. Germline deficiency of the cell surface receptor chain ST2 abrogated the mm IL-33-induced Th2-associated effects (pulmonary eosinophilia, goblet cell hyperplasia, and increased IL-4 and IL-5), yet the lymphocytic infiltration induced by full-length mouse IL-33 or mm IL-33 was not fully abrogated by the absence of ST2. The similar effects of IL-33 isoforms were associated with comparable regulation of gene expression, notably matrix metalloproteinases 3, 10, and 13. Thus, full-length IL-33 is functionally active in vivo in an ST2-independent fashion, and its effects are partially different from those of mature IL-33. The different effects of these isoforms, particularly the pro-Th2 effects of mature IL-33, are due to differential utilization of the IL-33R chain ST2, whereas their similar effects result from regulation of gene expression.
ISSN	00221767
e-ISSN	15506606
DOI	10.4049/jimmunol.1200259
Journal	The Journal of Immunology
Issue Number	1
Volume Number	189
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2012-07-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Inflammation Mediators Adverse Effects Interleukins Receptors, Cell Surface Physiology Receptors, Interleukin Th2 Cells Immunology Pathology Animals Carcinoma, Non-small-cell Lung Metabolism Cell Line, Tumor Gene Expression Regulation Genetics Hek293 Cells Administration & Dosage Interleukin-33 Biosynthesis Lung Neoplasms Mice Mice, Inbred Balb C Mice, Inbred C57bl Mice, Knockout Protein Biosynthesis Pulmonary Fibrosis Deficiency Stem Cells Comparative Study Research Support, N.i.h., Extramural Research Support, U.s. Gov't, Non-p.h.s. Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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