Anti-IL27 (full length) polyclonal antibody [Biotin]

Name: Anti-IL27 (full length) polyclonal antibody [Biotin]
SKU: DPABH-28401
Rating: 5 (1 reviews)

Rabbit Anti-Mouse IL27 (full length) polyclonal antibody for WB

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COA

SDS

Datasheet

Summary

Specifications

Antibody Isotype

IgG

Species Reactivity

Mouse

Immunogen

Recombinant full length Mouse IL27 protein.

Conjugate

Biotin

Applications

Application Notes

WB: 1/2000 - 1/10000.

Target

Alternative Names

IL27; interleukin 27; interleukin-27 subunit alpha; IL27-A; IL-27-A; interleukin 30; IL-27 p28 subunit; IL-27 subunit alpha; p28; Il30; IL-27; IL-27p28;

Entrez Gene ID

246779

UniProt ID

Q8K3I6

Product Background

Antigen Description

Cytokine with pro- and anti-inflammatory properties, that can regulate T helper cell development, suppress T-cell proliferation, stimulate cytotoxic T cell activity, induce isotype switching in B-cells, and that has diverse effects on innate immune cells. Among its target cells are CD4 T helper cells which can differentiate in type 1 effector cells (TH1), type 2 effector cells (TH2) and IL17 producing helper T-cells (TH17). It drives rapid clonal expansion of naive but not memory CD4 T-cells. It also strongly synergizes with IL-12 to trigger interferon-gamma/IFN-gamma production of naive CD4 T-cells, binds to the cytokine receptor WSX-1/TCCR which appears to be required but not sufficient for IL-27-mediated signal transduction. IL-27 potentiate the early phase of TH1 response and suppress TH2 and TH17 differentiation. It induces the differentiation of TH1 cells via two distinct pathways, p38 MAPK/TBX21- and ICAM1/ITGAL/ERK-dependent pathways. It also induces STAT1, STAT3, STAT4 and STAT5 phosphorylation and activates TBX21/T-Bet via STAT1 with resulting IL12RB2 up-regulation, an event crucial to TH1 cell commitment. It suppresses the expression of GATA3, the inhibitor TH1 cells development. In CD8 T-cells, it activates STATs as well as GZMB. IL-27 reveals to be a potent inhibitor of TH17 cell development and of IL-17 production. Indeed IL-27 subunit p28 alone is also able to inhibit the production of IL17 by CD4 and CD8 T-cells. While IL-27 suppressed the development of proinflammatory Th17 cells via STAT1, it inhibits the development of anti-inflammatory inducible regulatory T-cells, iTreg, independently of STAT1. IL-27 has also an effect on cytokine production, it suppresses proinflammatory cytokine production such as IL2, IL4, IL5 and IL6 and activates suppressors of cytokine signaling such as SOCS1 and SOCS3. Apart from suppression of cytokine production, IL-27 also antagonizes the effects of some cytokines such as IL6 through direct effects on T cells. Another important role of IL-27 is its antitumor activity as well as its antiangiogenic activity with activation of production of antiangiogenic chemokines such as IP-10/CXCL10 and MIG/CXCL9. In vein endothelial cells, it induces IRF1/interferon regulatory factor 1 and increase the expression of MHC class II transactivator/CIITA with resulting up-regulation of major histocompatibility complex class II. IL-27 also demonstrates antiviral activity with inhibitory properties on HIV-1 replivation.

Citations

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Documents

pdf COA

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References

High-Resolution Profiling of Innate Immune Responses by Porcine Dendritic Cell Subsetsin vitroandin vivo

FRONTIERS IN IMMUNOLOGY

Authors: Auray, Gael; Talker, Stephanie C.; Keller, Irene; Python, Sylvie; Gerber, Markus; Liniger, Matthias; Ganges, Llilianne; Bruggmann, Remy; Ruggli, Nicolas; Summerfield, Artur

Abstract

The present study investigated the transcriptomic response of porcine dendritic cells (DC) to innate stimulationin vitroandin vivo. The aim was to identify DC subset-specialization, suitable Toll-like receptor (TLR) ligands targeting plasmacytoid DC (pDC), and the DC activation profile during highly and low virulent classical swine fever virus (CSFV, strain Eystrup and Pinar del Rio, respectively) infection, chosen as model for a virus causing a severe immunopathology. After identification of porcine conventional DC (cDC) 1, cDC2, pDC and a monocyte-derived subset in lymphoid tissues, we characterized DC activation using transcriptomics, and focused on chemokines, interferons, cytokines, as well as on co-stimulatory and inhibitory molecules. We demonstrate that porcine pDC provide important signals for Th1 and interferon responses, with CpG triggering the strongest responses in pDC. DC isolated early after infection of pigs with either of the two CSFV strains showed prominent upregulation ofCCL5, CXCL9, CXCL10, CXCL11, andXCL1, as well as of the cytokinesTNFSF13B, IL6, IL7, IL12B, IL15, IL27. Transcription ofIL12Band many interferon genes were mostly restricted to pDC. Interestingly, the infection was associated with a prominent induction of inhibitory and cell death receptors. When comparing low and highly virulent CSFV strains, the latter induced a stronger inflammatory and antiviral response but a weaker cell cycle response, and reduced antigen presentation functions of DC. Taken together, we provide high-resolution information on DC activation in pigs, as well as information on how DC modulation could be linked to CSFV immunopathology.

Lithium Controls Central Nervous System Autoimmunity through Modulation of IFN-gamma Signaling

PLOS ONE

Authors: Rowse, Amber L.; Naves, Rodrigo; Cashman, Kevin S.; McGuire, Donald J.; Mbana, Tethia; Raman, Chander; De Sarno, Patrizia

Abstract

Inhibitors of glycogen synthase kinase 3 (GSK3) are being explored as therapy for chronic inflammatory diseases. We previously demonstrated that the GSK inhibitor lithium is beneficial in experimental autoimmune encephalomyelitis (EAE), the mouse model of multiple sclerosis. In this study we report that lithium suppresses EAE induced by encephalitogenic interferon-gamma (IFN-gamma)-producing T helper (Th1) cells but not by interleukin (IL)-17-producing T helper (Th17) cells. The therapeutic activity of lithium required functional IFN-gamma-signaling, but not the receptor for type I IFN (IFNAR). Inhibitor/s of GSK3 attenuated IFN-gamma dependent activation of the transcription factor STAT1 in naive T cells as well as in encephalitogenic T cells and Th1 cells. The inhibition of STAT1 activation was associated with reduced IFN-gamma production and decreased expansion of encephalitogenic Th1 cells. Furthermore, lithium treatment induced Il27 expression within the spinal cords of mice with EAE. In contrast, such treatment of Ifngr(-)/(-) mice did not induce Il27 and was associated with lack of therapeutic response. Our study reveals a novel mechanism for the efficacy of GSK3 targeting in EAE, through the IFN-gamma-STAT1 axis that is independent IFNAR-STAT1 axis. Overall our findings set the framework for the use of GSK3 inhibitors as therapeutic agents in autoimmune neuroinflammation.