Anti-IL31 polyclonal antibody

Type I cytokine receptors mediate the action of the members of the long chain cytokines canonically involved in numerous physiological function. Here we report a novel cytokine receptor termed Japanese flounder glycoprotein 130 homologue or JfGPH, exhibiting the unique type I cytokine receptor motifs i.e. having a cytokine binding domain (CBD) containing two pairs of conserved cysteine (C) residues. a WSXWS motif, three fibronectin domains all in the extracellular region. It is also composed of the Jak binding domains Box I and Box 2, and a STAT 3 binding motif (Box 3) in the cytoplasmic region suggesting its mediatory role for Janus kinase/Signal transducers and activators of transcription (Jak/STAT) signal pathway. The JfGPH cDNA is about 3 kb encoding 801 amino acid residues with a predicted molecular weight of 90 kDa and its gene has an 11-exon/10-intron architecture. While JfGPH shows significant homology with the members of type-1 cytokine receptor family including IL6ST (or gp 130), IL31 alpha (or GLMR), CSF3R (or GCSFR), LIFR, OSMR, IL12R beta 1 and LEPR, structural and phylogenetic analysis of its protein revealed that it is a novel and an-ancestral cytokine receptor found in teleost. JfGPH gene is ubiquitously expressed in Japanese flounder tissues and in a natural embryo (HINAE) cell line showing its critical role in teleost physiological functions similar to gp 130 in higher vertebrates. High expression of JfGPH transcripts in immune-related tissues and, in ovary and embryo-derived cell line suggest its role in immune responses, and reproduction/development, respectively. In vitro stimulation of spleen, kidney, peripheral blood leukocytes (PBLs) and HINAE revealed that JfGPH is down-regulated by polyinosinic:polycytidylic acid (poly I:C), an interferon (IFN) inducer, suggesting an apparent control of the JfGPH's expression during IFN-induced Jak/STAT signaling. (c) 2007 Elsevier Ltd. All rights reserved.

BackgroundInterleukin (IL)-31 is implicated in pruritus associated with pruritic skin diseases like atopic dermatitis. Although pruritus is a prominent feature in dermatomyositis (DM), few studies have evaluated the pathogenesis of DM-associated itch. ObjectivesTo establish the prevalence of itch in DM, and to investigate the role of IL-31 in DM-related itch. MethodsPruritus and disease activity of DM were evaluated by a visual analogue scale (VAS) and the Cutaneous Disease and Activity Severity Index (CDASI), respectively. Expression of IL-31 and IL-31 receptor alpha (IL-31RA) in lesional DM, nonlesional DM and healthy control skin was evaluated by quantitative reverse-transcriptase polymerase chain reaction and immunofluorescence. Flow cytometry was performed on skin cells isolated from lesional DM skin to identify cellular sources of IL-31 in DM. ResultsAmong 191 patients with DM, 508% had moderate-to-severe itch, and itch was correlated with increased cutaneous severity (r = 034). In patients with itchy DM, gene expression of IL31 and IL31RA in lesional skin was upregulated compared with nonlesional skin and healthy control skin. IL31 mRNA expression positively correlated with VAS itch score (r = 067). On immunofluorescence, immunoreactivity for IL-31 and IL-31RA was stronger in lesional skin. Flow cytometry showed that lesional DM skin contained significantly more IL-31-producing cells, and CD4(+) cells were the most common cell type. Lenabasum, an emerging treatment for DM, significantly downregulated IL-31 from CpG-stimulated peripheral blood mononuclear cells. ConclusionsIncreased skin IL-31 may play a role in DM-associated itch, and ongoing trials will evaluate the effects of systemic treatment on IL-31 and itch in DM.