@Article{ecn.2011.0288,
AUTHOR = {Diana Boraschi, Davide Lucchesi, Stefan Hainzl, Maria Leitner, Elisabeth Maier, Doris Mangelberger, Gertie J. Oostingh, Tobias Pfaller, Claudia Pixner, Gernot Posselt, Paola Italiani, Marcel F. Nold, Claudia A. Nold-Petry, Philip Bufler, Charles A. Dinarello},
TITLE = {IL-37: a new anti-inflammatory cytokine of the IL-1 family},
JOURNAL = {European Cytokine Network},
VOLUME = {22},
YEAR = {2011},
NUMBER = {3},
PAGES = {127--47},
URL = {http://www.techscience.com/ECN/v22n3/65817},
ISSN = {1952-4005},
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.},
DOI = {10.1684/ecn.2011.0288}
}