Structure and function of interleukin-22 and other members of the interleukin-10 family

Abstract

The IL-10 family of cytokines is comprised of IL-10, . The IL-10 family members bind to shared class II cytokine receptor chains that associate in various combinations in heterodimeric complexes. Upon interleukin/receptor complex formation, these proteins switch on the Jak/STAT pathway and elicit pleiotropic biological responses whose variety sharply contrasts with their structural similarities. IL-10 family members are involved in several human diseases and health conditions and hence their structural analyses may provide valuable information to design specific therapeutic strategies. In this review, we describe the human interleukin-10 family of cytokines, focusing on their structures and functions, with particular attention given to IL-22 and IL-10. We report on the recently published structures of IL-10 cytokine family members and their complexes with cognate transmembrane and soluble receptors as well as on interleukin physiology and physiopathology.

Modulatory effect of celastrol on Th1/Th2 cytokines profile, TLR2 and CD3+ T-lymphocyte expression in a relapsing–remitting model of multiple sclerosis in rats

“…TNF-α mediates inflammatory reaction by altering the blood brain barrier, influences lymphocyte behavior, and induces tissue damage with astrogliosis and destruction of oligodendrocytes (Issazadeh et al, 1995;Montgomery and Bowers, 2012). The anti-inflammatory and immunoregulatory effect of IL-10 could be contributed to downregulation of Th1 inflammatory cytokines expression, enhancing B cell survival and antibody production, blocking NF-κB activity and promoting tissue repair (Trivella et al, 2010). The preliminary evidence showed that B cells from multiple sclerosis patients produce decreased amounts of IL-10 suggesting its regulatory role (Duddy et al, 2007).…”

The crystal structure of zebrafish IL-22 reveals an evolutionary, conserved structure highly similar to that of human IL-22

“…7,[51][52][53] Phylogeny of class II cytokines The phylogeny of class II cytokines has been the subject of substantial debate. 2,[11][12][13][14][15][16][17]22 Most of the conclusions were drawn from sequence alignments and subsequent calculation of phylogenetic trees.…”

Oncostatin M overexpression induces skin inflammation but is not required in the mouse model of imiquimod‐induced psoriasis‐like inflammation

“…Within the family of IL-10 cytokines, IL-22 is preferentially secreted by Th17 cells while IL-19, IL-20, and IL-24 are mostly produced by keratinocytes, secondarily to Th17-related cytokine stimulation [37,38]. All these cytokines were described to involve STAT3 signaling [39] and to play a redundant role in the alteration of epidermis functions [40], which might contribute together, with IL-6, to compensate the absence of OSM activity.The lack of requirement of OSM in the induction of the IMQ model could also be explained by its strong dependence on the IL-23/IL-17 axis [13]. Both cytokines were found upregulated in a similar manner in all groups of IMQ-treated mice.…”