Journal ArticleDOI
Disease-associated functions of IL-33: the new kid in the IL-1 family.
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TLDR
IL-33 is host-protective against helminth infection and reduces atherosclerosis by promoting TH2-type immune responses but can also promote the pathogenesis of asthma by expanding TH2 cells and mediate joint inflammation, atopic dermatitis and anaphylaxis by mast cell activation.Abstract:
Interleukin-33 (IL-33), a newly described member of the IL-1 family, is expressed by many cell types following pro-inflammatory stimulation and is thought to be released on cell lysis. The IL-33 receptor, consisting of ST2 and IL-1 receptor accessory protein, is also widely expressed, particularly by T helper 2 (T(H)2) cells and mast cells. IL-33 is host-protective against helminth infection and reduces atherosclerosis by promoting T(H)2-type immune responses. However, IL-33 can also promote the pathogenesis of asthma by expanding T(H)2 cells and mediate joint inflammation, atopic dermatitis and anaphylaxis by mast cell activation. Thus IL-33 could be a new target for therapeutic intervention across a range of diseases.read more
Citations
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Journal ArticleDOI
The Interleukin-1 Family: Back to the Future
TL;DR: The key properties of IL-1 family members are reviewed, with emphasis on pathways of negative regulation and orchestration of innate and adaptive immunity.
Journal ArticleDOI
Innate and adaptive immune responses in asthma
TL;DR: Recent advances in understanding of the sentinel role played by innate immunity provides new targets for disease prevention and treatment that include pathways of innate stimulation by environmental or endogenous pathogen-associated molecular patterns (PAMPs) and danger-associated Molecular patterns (DAMPs), and the identification of new T cell subsets and lymphoid cells.
Journal ArticleDOI
IL-33 is a crucial amplifier of innate rather than acquired immunity
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 +13 more
TL;DR: It is 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 andIL-33 was important for innate-type mucosal immunity in the lungs and gut.
Journal ArticleDOI
The many paths to asthma: phenotype shaped by innate and adaptive immunity
TL;DR: Animal models of asthma have helped to clarify some of the underlying mechanisms of asthma, demonstrating the importance of T helper type 2 (TH2)-driven allergic responses, as well as of the non-allergic and intrinsic pathways, and contributing to understanding of the heterogeneity of asthma.
Journal ArticleDOI
IL-33: an alarmin cytokine with crucial roles in innate immunity, inflammation and allergy.
TL;DR: The cellular sources, mode of action and regulation of IL-33 are discussed, and its crucial roles in vivo are highlighted with particular emphasis on results obtained using IL33-deficient mice.
References
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Journal ArticleDOI
Release of chromatin protein HMGB1 by necrotic cells triggers inflammation
TL;DR: It is reported that Hmgb1-/- necrotic cells have a greatly reduced ability to promote inflammation, which proves that the release of HMGB1 can signal the demise of a cell to its neighbours, and cells undergoing apoptosis are programmed to withhold the signal that is broadcast by cells that have been damaged or killed by trauma.
Journal ArticleDOI
IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines
Jochen Schmitz,Alexander Owyang,Elizabeth R. Oldham,Yaoli Song,Erin Murphy,Terril K. McClanahan,Gerard Zurawski,Mehrdad M. Moshrefi,Jinzhong Qin,Xiaoxia Li,Daniel M. Gorman,J. Fernando Bazan,Robert A. Kastelein +12 more
TL;DR: A member of theIL-1 family, IL-33, which mediates its biological effects via IL-1 receptor ST 2, activates NF-kappaB and MAP kinases, and drives production of T(H)2-associated cytokines from in vitro polarized T( H)2 cells is reported.
Journal ArticleDOI
DAMPs, PAMPs and alarmins: all we need to know about danger
TL;DR: The term “alarmin” is proposed to categorize such endogenous molecules that signal tissue and cell damage, and can be considered subgroups of a larger set, the damage‐associated molecular patterns (DAMPs).
Journal ArticleDOI
The IL-1-Like Cytokine IL-33 Is Constitutively Expressed in the Nucleus of Endothelial Cells and Epithelial Cells In Vivo : A Novel ‘Alarmin’?
Christine Moussion,Nathalie Ortega,Nathalie Ortega,Jean-Philippe Girard,Jean-Philippe Girard +4 more
TL;DR: It is speculated that IL-33 may function, similarly to the prototype ‘alarmin’ HMGB1, as an endogenous ‘danger’ signal to alert the immune system after endothelial or epithelial cell damage during trauma or infection.
Journal ArticleDOI
IL-33, the IL-1-like cytokine ligand for ST2 receptor, is a chromatin-associated nuclear factor in vivo
Virginie Carriere,Lucie Roussel,Nathalie Ortega,Delphine-Armelle Lacorre,Laure Americh,Luc Aguilar,Gérard Bouche,Jean-Philippe Girard +7 more
TL;DR: In situ hybridization demonstrated that endothelial cells constitute a major source of IL-33 mRNA in chronically inflamed tissues from patients with rheumatoid arthritis and Crohn's disease, and data suggest thatIL-33 is a dual function protein that may function as both a proinflammatory cytokine and an intracellular nuclear factor with transcriptional regulatory properties.