Structures and biological functions of IL-31 and IL-31 receptors.

Division of Medical Cell Biology, College of Life Sciences, Sichuan University, Chengdu, PR China.
Cytokine & growth factor reviews (Impact Factor: 6.54). 11/2008; 19(5-6):347-56. DOI: 10.1016/j.cytogfr.2008.08.003
Source: PubMed

ABSTRACT Interleukin-31, produced mainly by activated CD4(+) T cells, is a newly discovered member of the gp130/IL-6 cytokine family. Unlike all the other family members, IL-31 does not engage gp130. Its receptor heterodimer consists of a unique gp130-like receptor chain IL-31RA, and the receptor subunit OSMRbeta that is shared with another family member oncostatin M (OSM). Binding of IL-31 to its receptor activates Jak/STAT, PI3K/AKT and MAPK pathways. IL-31 acts on a broad range of immune- and non-immune cells and therefore possesses potential pleiotropic physiological functions, including regulating hematopoiesis and immune response, causing inflammatory bowel disease, airway hypersensitivity and dermatitis. This review summarizes the recent findings on the biological characterization and physiological roles of IL-31 and its receptors.

1 Follower
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background Severe pruritus is one of the cardinal symptoms of atopic dermatitis (AD). Recently, the interleukin (IL)-31 cytokine has been implicated in the induction and maintenance of severe pruritus and chronic skin inflammation in several pruritic skin diseases, including AD.Objective We aimed to investigate the association of the IL-31 gene haplotypes with pruritus and severity of AD, as well as their correlation to the serum IL-31 levels.MethodsA total of 127 patients with AD and 96 healthy controls were analyzed for polymorphic variants of the IL-31 gene using an amplification refractory mutation system–polymerase chain reaction method. IL-31 haplotype frequencies were estimated with the use of tagging single nucleotide polymorphisms, expectation-maximization, and Excoffier–Laval–Balding algorithms. Serum IL-31 levels were measured using a standard enzyme-linked immunosorbent assay kit.ResultsThe frequency of AAG, AGA, AGG, and GAA haplotypes of the IL-31 gene was higher in patients with AD than in controls. The mean IL-31 levels in serum were lower in controls than in the patients (P < 0.00001) and were higher in those with severe vs. mild AD (P = 0.008). No correlation was found between IL-31 and the severity of pruritus. The haplotype AAA was associated with a high IL-31 serum level (P = 0.008) and with severe AD (high SCORing Atopic Dermatitis index) (P = 0.013). The haplotype GAA was associated with a severe form of pruritus (P = 0.016) and the haplotype GGG with the mild one (P = 0.07).Conclusion The results of this study suggest that the severity of AD in a Polish population is associated with some specific haplotypes of the IL-31 gene, which can indicate their prognostic role also renews the questions concerning the role of IL-31 in pruritus in AD.
    International journal of dermatology 01/2015; 54(1). DOI:10.1111/ijd.12666 · 1.23 Impact Factor
  • [Show abstract] [Hide abstract]
    ABSTRACT: IL-31, predominantly produced by CD45RO + CLA + Th2 cells, plays an important pathogenetic role in pruritic skin diseases like atopic dermatitis. As tumor cells in Sézary syndrome (SS) and Mycosis fungoides (MF) possess similar immunophenotypes and the conditions mentioned are often associated with pruritus, the analysis of the IL-31 pathway in MF/SS patients is of interest. Serum samples from the peripheral blood of 23 patients and 17 controls were analyzed for IL-31 abundance and correlated with disease stage and pruritus. Furthermore IL-31-, IL-31 receptor alpha (IL-31Rα)- and Oncostatin M receptor beta (OSMRβ)-mRNA expression was measured in blood tumor cells from SS patients, memory T-cells from controls and lymphoma cell lines. Serum IL-31 levels were low but differed between groups with no or strong pruritus. Expression of IL-31 was detectable at low levels in cell lines, but not in the tumor cells of SS patients. Stimulation with PMA/ionomycin led to indiscriminate expression in peripheral blood tumor cells and control T-cells. IL-2-stimulation resulted in expression only in 9/11 patient samples. IL-31Rα-expression was detectable in 10/10 cell lines, 8/15 peripheral blood samples from SS patients, and 4/10 controls; whereas, OSMRβ mRNA was detectable in 4/10 cell lines, but only one patient and control sample. The results of our analyses regarding serum levels and receptor expression do not suggest a central role of IL-31 in MF/SS pathogenesis. However, the results of IL-2 stimulation as well as the increased IL-31 levels in patients with strong pruritus offer a rationale for therapeutic approach in this subset of patients.
    Archives for Dermatological Research 12/2014; DOI:10.1007/s00403-014-1527-x · 2.27 Impact Factor
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Objective. Chemokines exert different inflammatory responses which can potentially be related to certain fetal chromosomal abnormalities. The aim of the study was to determine the concentration of selected chemokines in plasma and amniotic fluid of women with fetal Down syndrome. Method. Out of 171 amniocentesis, we had 7 patients with confirmed fetal Down syndrome (15th-18th weeks of gestation). For the purpose of our control, we chose 14 women without confirmed chromosomal aberration. To assess the concentration of chemokines in the blood plasma and amniotic fluid, we used a protein macroarray, which allows the simultaneous determination of 40 chemokines per sample. Results. We showed significant decrease in the concentration of 4 chemokines, HCC-4, IL-28A, IL-31, and MCP-2, and increase in the concentration of CXCL7 (NAP-2) in plasma of women with fetal Down syndrome. Furthermore, we showed decrease in concentration of 3 chemokines, ITAC, MCP-3, MIF, and increase in concentration of 4 chemokines, IP-10, MPIF-1, CXCL7, and 6Ckine, in amniotic fluid of women with fetal Down syndrome. Conclusion. On the basis of our findings, our hypothesis is that the chemokines may play role in the pathogenesis of Down syndrome. Defining their potential as biochemical markers of Down syndrome requires further investigation on larger group of patients.
    Mediators of Inflammation 11/2014; 2014:835837. DOI:10.1155/2014/835837 · 2.42 Impact Factor


Available from