| IL-33 is a crucial amplifier of innate rather than acquired immunity. | |
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MedLine Citation:
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PMID: 20937871 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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IL-33, a member of the IL-1-related cytokines, is considered to be a proallergic cytokine that is especially involved in Th2-type immune responses. Moreover, like IL-1α, IL-33 has been suggested to act as an "alarmin" that amplifies immune responses during tissue injury. In contrast to IL-1, however, the precise roles of IL-33 in those settings are poorly understood. Using IL-1- and IL-33-deficient mice, we found that IL-1, but not IL-33, played a substantial role in induction of T cell-mediated type IV hypersensitivity such as contact and delayed-type hypersensitivity and autoimmune diseases such as experimental autoimmune encephalomyelitis. Most notably, however, IL-33 was important for innate-type mucosal immunity in the lungs and gut. That is, IL-33 was essential for manifestation of T cell-independent protease allergen-induced airway inflammation as well as OVA-induced allergic topical airway inflammation, without affecting acquisition of antigen-specific memory T cells. IL-33 was significantly involved in the development of dextran-induced colitis accompanied by T cell-independent epithelial cell damage, but not in streptozocin-induced diabetes or Con A-induced hepatitis characterized by T cell-mediated apoptotic tissue destruction. In addition, IL-33-deficient mice showed a substantially diminished LPS-induced systemic inflammatory response. These observations indicate that IL-33 is a crucial amplifier of mucosal and systemic innate, rather than acquired, immune responses. |
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Authors:
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Keisuke Oboki; Tatsukuni Ohno; Naoki Kajiwara; Ken Arae; Hideaki Morita; Akina Ishii; Aya Nambu; Takaya Abe; Hiroshi Kiyonari; Kenji Matsumoto; Katsuko Sudo; Ko Okumura; Hirohisa Saito; Susumu Nakae |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't Date: 2010-10-11 |
Journal Detail:
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Title: Proceedings of the National Academy of Sciences of the United States of America Volume: 107 ISSN: 1091-6490 ISO Abbreviation: Proc. Natl. Acad. Sci. U.S.A. Publication Date: 2010 Oct |
Date Detail:
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Created Date: 2010-10-27 Completed Date: 2010-11-22 Revised Date: 2011-07-28 |
Medline Journal Info:
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Nlm Unique ID: 7505876 Medline TA: Proc Natl Acad Sci U S A Country: United States |
Other Details:
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Languages: eng Pagination: 18581-6 Citation Subset: IM |
Affiliation:
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Department of Allergy and Immunology, National Research Institute for Child Health and Development, Tokyo 157-8535, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Adaptive Immunity Animals Autoimmunity Colitis / etiology, immunology Immunity, Innate* Immunity, Mucosal Interleukin-1 / deficiency, genetics, immunology Interleukins / deficiency, genetics, immunology* Lipopolysaccharides / toxicity Mice Mice, Inbred BALB C Mice, Inbred C57BL Mice, Knockout Ovalbumin / immunology Respiratory Hypersensitivity / etiology, immunology, pathology Shock, Septic / etiology, immunology |
| Chemical | |
Reg. No./Substance:
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0/Interleukin-1; 0/Interleukins; 0/Lipopolysaccharides; 0/interleukin-33, mouse; 9006-59-1/Ovalbumin |
| Comments/Corrections | |
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