IL-37: a new anti-inflammatory cytokine of the IL-1 family |
| |
Authors: | Boraschi Diana Lucchesi Davide Hainzl Stefan Leitner Maria Maier Elisabeth Mangelberger Doris Oostingh Gertie J Pfaller Tobias Pixner Claudia Posselt Gernot Italiani Paola Nold Marcel F Nold-Petry Claudia A Bufler Philip Dinarello Charles A |
| |
Affiliation: | Laboratory of Innate Immunity and Cytokines, Institute of Biomedical Technologies, National Research Council, I-56124 Pisa, Italy. diana.boraschi@itb.cnr.it |
| |
Abstract: | The IL-1 family of cytokines encompasses eleven proteins that each share a similar β-barrel structure and bind to Ig-like receptors. Some of the IL-1-like cytokines have been well characterised, and play key roles in the development and regulation of inflammation. Indeed, IL-1α (IL-1F1), IL-1β (IL-1F2), and IL-18 (IL-1F4) are well-known inflammatory cytokines active in the initiation of the inflammatory reaction and in driving Th1 and Th17 inflammatory responses. In contrast, IL-1 receptor antagonist (IL-1Ra, IL-1F3) and the receptor antagonist binding to IL-1Rrp2 (IL-36Ra, IL-1F5) reduce inflammation by blocking the binding of the agonist receptor ligands. In the case of IL-37 (IL-1F7), of which five different splice variants have been described, less is known of its function, and identification of the components of a heterodimeric receptor complex remains unclear. Some studies suggest that IL-37 binds to the α chain of the IL-18 receptor in a non-competitive fashion, and this may explain some of the disparate biological effects that have been reported for mice deficient in the IL-18R. The biological properties of IL-37 are mainly those of down-regulating inflammation, as assessed in models where human IL-37 is expressed in mice. In this review, an overview of the role of IL-37 in the regulation of inflammation is presented. The finding that IL-37 also locates to the nucleus, as do IL-1α and IL-33, for receptor-independent organ/tissue-specific regulation of inflammation is also reviewed. |
| |
Keywords: | |
本文献已被 PubMed 等数据库收录! |
|