Journal ArticleDOI
The IL-1 family of cytokines and receptors in rheumatic diseases.
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TLDR
The main functions of the IL-1 family are innate immune reactions and inflammation, rather than acquired immunity, which can occur in several rheumatic diseases.Abstract:
More than any other cytokine family, the 11 members of the IL-1 family are associated with innate immune responses, which occur in acute inflammation and chronic inflammatory conditions such as rheumatic diseases. In many rheumatic diseases, the severity of the condition can result from the balance between the pro-inflammatory and anti-inflammatory members of the IL-1 family. Pro-inflammatory family members (IL-1α, IL-1β, IL-18, IL-33, IL-36α, IL-36β and IL-36γ) are found in the articular environment during arthritis and often correlate with the degree of inflammation present. IL-1β has emerged as pivotal for promoting inflammation, particularly in autoinflammatory diseases, whereas IL-1α and the IL-36 subfamily are associated with skin diseases. IL-33 regulates T helper 2 (TH2) cell-mediated diseases, in sharp contrast to IL-18, which mainly regulates TH1 cell-mediated responses. The IL-1 family also contains four members that suppress inflammation: two specific receptor antagonists (IL-1 receptor antagonist (IL-1Ra) and IL-36 receptor antagonist (IL-36Ra)), and two members that broadly suppress innate inflammation by non-specifically reducing several cytokines and chemokines (IL-37 and IL-38). In this Review, each of the eleven IL-1 family cytokines and their receptors are discussed, along with their putative roles in rheumatic disease and therapeutic options for targeting or promoting these cytokines. Cytokines from the IL-1 family perform important functions in innate immune reactions, but can also be involved in chronic inflammatory diseases. This Review highlights the roles of IL-1 family members in rheumatic diseases and potential therapeutic approaches to targeting them.read more
Citations
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Early IL-1 receptor blockade in severe inflammatory respiratory failure complicating COVID-19.
Raphael Cauchois,Marie Koubi,David Delarbre,Cecile Manet,Julien Carvelli,Valery Benjamin Blasco,Rodolphe Jean,Louis Fouche,Charleric Bornet,Vanessa Pauly,Karin Mazodier,Vincent Pestre,Pierre André Jarrot,Charles A. Dinarello,Gilles Kaplanski +14 more
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Journal ArticleDOI
Biologic basis for interleukin-1 in disease
TL;DR: This is a lengthy review, with 586 citations chosen to illustrate specific areas of interest rather than a compendium of references, which summarizes what the author considers established or controversial topics linking the biology of IL-1 to mechanisms of disease.
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.
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