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IK cytokine, down_regulator of HLA II

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[# NB100-88125 ] IK cytokine, down_regulator of HLA II


NB100-88125 | IK cytokine, down_regulator of HLA II , 0.1 ml
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(1) Identification of potential embryokines in the bovine reproductive tract.[TOP]

Pubmed ID :29128220
Publication Date : //
Knowledge of the molecules used by the maternal reproductive tract to regulate development of the preimplantation embryo is largely incomplete. The goal of the present experiment was to identify candidates for this function. The approach was to assess expression patterns in the endometrium and oviduct of 93 genes encoding for hormones, growth factors, chemokines, cytokines, and WNT-related molecules. Results show that all of the genes were expressed in the reproductive tract. Expression in oviduct was affected by day of the estrous cycle for 21 genes with 11 genes having highest expression at estrus (CCL21, CTGF, CXCL10, CXCL16, DKK3, FGF10, IL18, IL33, IL34, PGF, and SFRP2), 1 gene at d 3 (WNT4), 8 at d 5 (BMP7, HGF, IL6, SFRP1, TGFB1, WIF1, WNT2, and WNT5A), and 1 at d 7 (IK). For endometrium, expression of 34 genes was affected by day of the estrous cycle with 11 having highest expression at d 0 (BMP7, CCL14, CCL21, CCL26, CTGF, CXCL12, IGF2, IL16, IL33, SFRP2, and WIF1), 2 at d 3 (HDGF, IL15), 14 at d 5 (CSF2, CX3CL1, CXCL3, FGF1, FGF2, GRO1, HGF, IGF1, IL1B, IL8, SFRP1, SFRP4, WNT5A, and WNT16), and 7 at d 7 (CXCL16, FGF13, HDGFRP2, TDGF1, VEGFB, WNT7A, and WNT11). Results are consistent with a set of genes regulated by estradiol early in the estrous cycle and another set regulated by progesterone later in the cycle. The cell-signaling genes identified here as being expressed in the oviduct and endometrium could serve to regulate early embryonic development in a stage-of-pregnancy-specific manner.

Authors : Tríbulo P, Siqueira L G B, Oliveira L J, Scheffler T, Hansen P J,

(2) Therapeutic Effect of Exogenous Truncated IK Protein in Inflammatory Arthritis.[TOP]

Pubmed ID :28906466
Publication Date : //
Inhibitor K562 (IK) protein was first isolated from the culture medium of K562, a leukemia cell line. It is known to be an inhibitory regulator of interferon-γ-induced major histocompatibility complex class (MHC) II expression. Previously, we found that transgenic (Tg) mice constitutively expressing truncated IK (tIK) showed reduced numbers of pathogenic Th1 and Th17 cells, which are known to be involved in the development of rheumatoid arthritis (RA). Here, we investigated whether exogenous tIK protein has a therapeutic effect in arthritis in disease models and analyzed its mechanism. Exogenous tIK protein was produced in an insect expression system and applied to the collagen antibody-induced arthritis (CAIA) mouse disease model. Injection of tIK protein alleviated the symptoms of arthritis in the CAIA model and reduced Th1 and Th17 cell populations. In addition, treatment of cultured T cells with tIK protein induced expression of A20, a negative regulator of nuclear factor-κB (NFκB)-induced inflammation, and reduced expression of several transcription factors related to T cell activation. We conclude that exogenous tIK protein has the potential to act as a new therapeutic agent for RA patients, because it has a different mode of action to biopharmaceutical agents, such as tumor necrosis factor antagonists, that are currently used to treat RA.

Authors : Choi Seulgi, Park HyeLim, Jung SeoYeon, Kim Eun-Kyung, Cho Mi-La, Min Jun-Ki, Moon Su-Jin, Lee Sang-Myeong, Cho Jang-Hee, Lee Dong-Hee, Nam Jae-Hwan,

(3) Pan-PPAR agonist IVA337 is effective in experimental lung fibrosis and pulmonary hypertension.[TOP]

Pubmed ID :28801346
Publication Date : //
To evaluate the antifibrotic effects of the pan-peroxisome proliferator-activated receptor (PPAR) agonist IVA337 in preclinical mouse models of pulmonary fibrosis and related pulmonary hypertension (PH).

Authors : Avouac Jerome, Konstantinova Irena, Guignabert Christophe, Pezet Sonia, Sadoine Jeremy, Guilbert Thomas, Cauvet Anne, Tu Ly, Luccarini Jean-Michel, Junien Jean-Louis, Broqua Pierre, Allanore Yannick,

(4) Defining the inflammatory signature of human lung explant tissue in the presence and absence of glucocorticoid.[TOP]

Pubmed ID :28721202
Publication Date : //
 Airway inflammation is a feature of many respiratory diseases and there is a need for newer, more effective anti-inflammatory compounds. The aim of this study was to develop an human lung explant model which can be used to help study the mechanisms underlying inflammatory responses and which can provide a tool to aid drug discovery for inflammatory respiratory diseases such as asthma and COPD.

Authors : Rimington Tracy L, Hodge Emily, Billington Charlotte K, Bhaker Sangita, K C Binaya, Kilty Iain, Jelinsky Scott, Hall Ian P, Sayers Ian,

(5) Recombinant Adeno-Associated Virus Expressing Truncated IK Cytokine Diminishes the Symptoms of Inflammatory Arthritis.[TOP]

Pubmed ID :28683532
Publication Date : //
IK can downregulate interferon-gamma-induced major histocompatibility complex (MHC) class II expression through the MHC class II transactivator, which suggests that IK can inhibit the interactions between immune cells. We delivered adeno-associated virus serotype 2 (AAV2) encoding the genes for truncated IK (tIK) or green fluorescent protein (GFP) to DBA1/J mice via intravenous injection. Seven weeks after injection, collagen-induced arthritis was induced in the AAV2-treated mice. AAV2-tIK injection reduced the severity of arthritis and the percentage of pathogenic Th17 cells compared with AAV2-GFP injection. These results suggest a novel gene therapy strategy for treatment of inflammatory arthritis.

Authors : Choi Seulgi, Park Hyelim, Minelko Marstella, Kim Eun-Kyung, Cho Mi-Ra, Nam Jae-Hwan,

(6) A functional SUMO-motif in the active site of PIM1 promotes its degradation via RNF4, and stimulates protein kinase activity.[TOP]

Pubmed ID :28620180
Publication Date : //
The PIM1 serine/threonine protein kinase mediates growth factor and survival signalling, and cooperates potently with c-MYC during tumorigenesis. PIM1 is overexpressed in many human cancers and is a promising target for drug development. PIM1 levels are regulated mainly through cytokine-induced transcription and protein degradation, but mechanisms regulating its activity and levels remain largely unexplored. Here, we show that PIM1 is modified in vitro and in cultured cells by the Small ubiquitin-like modifier (SUMO) on two independent sites: K169, within a consensus SUMOylation motif (IKDE) in the active site of PIM1, and also at a second promiscuous site. Alanine substitution of E171 (within the consensus motif) abolished SUMOylation, significantly increased the half-life of PIM1, and markedly reduced its ubiquitylation. Mechanistically, SUMOylation promoted ubiquitin-mediated degradation of PIM1 via recruitment of the SUMO-targeted ubiquitin ligase, RNF4. Additionally, SUMOylated PIM1 showed enhanced protein kinase activity in vitro. Interestingly, the E171A mutant was active in vitro but displayed altered substrate specificity in cultured cells, consistent with the idea that SUMOylation may govern PIM1 substrate specificity under certain contexts. Taken together, these data demonstrate that the protein kinase activity and levels of PIM1 can be regulated by a covalent post-translational modification.

Authors : Iyer R Sumanth, Chatham Lynsey, Sleigh Roger, Meek David W,

(7) Immunotherapies in neuromyelitis optica spectrum disorder: efficacy and predictors of response.[TOP]

Pubmed ID :28572277
Publication Date : //
To analyse predictors for relapses and number of attacks under different immunotherapies in patients with neuromyelitis optica spectrum disorder (NMOSD).

Authors : Stellmann Jan-Patrick, Krumbholz Markus, Friede Tim, Gahlen Anna, Borisow Nadja, Fischer Katrin, Hellwig Kerstin, Pache Florence, Ruprecht Klemens, Havla Joachim, Kümpfel Tania, Aktas Orhan, Hartung Hans-Peter, Ringelstein Marius, Geis Christian, Kleinschnitz Christoph, Berthele Achim, Hemmer Bernhard, Angstwurm Klemens, Young Kim Lea, Schuster Simon, Stangel Martin, Lauda Florian, Tumani Hayrettin, Mayer Christoph, Zeltner Lena, Ziemann Ulf, Linker Ralf Andreas, Schwab Matthias, Marziniak Martin, Then Bergh Florian, Hofstadt-van Oy Ulrich, Neuhaus Oliver, Zettl Uwe, Faiss Jürgen, Wildemann Brigitte, Paul Friedemann, Jarius Sven, Trebst Corinna, Kleiter Ingo, ,

(8) Comparison of the Anti-Inflammatory Activities of Supercritical Carbon Dioxide versus Ethanol Extracts from Leaves of Perilla frutescens Britt. Radiation Mutant.[TOP]

Pubmed ID :28218690
Publication Date : //
In this study, we aimed to compare supercritical carbon dioxide extraction and ethanol extraction for isoegomaketone (IK) content in perilla leaf extracts and to identify the optimal method. We measured the IK concentration using HPLC and inflammatory mediators in lipopolysaccharide (LPS)-stimulated RAW 264.7 cells from the extracts. The IK concentration was 10-fold higher in perilla leaf extracts by supercritical carbon dioxide extraction (SFE) compared with that in perilla leaf extracts by ethanol extraction (EE). When the extracts were treated in LPS-induced RAW 264.7 cells at 25 μg/mL, the SFE inhibited the expression of inflammatory mediators such as nitric oxide (NO), monocyte chemoattractant protein-1 (MCP-1), interleutkin-6 (IL-6), interferon-β (IFN-β), and inducible nitric oxide synthase (iNOS) to a much greater extent compared with EE. Taken together, supercritical carbon dioxide extraction is considered the optimal process for obtaining high IK content and anti-inflammatory activities in leaf extracts from the P. frutescens Britt. radiation mutant.

Authors : Jin Chang Hyun, Park Han Chul, So Yangkang, Nam Bomi, Han Sung Nim, Kim Jin-Baek,

(9) Stimulatory actions of a novel thiourea derivative on large-conductance, calcium-activated potassium channels.[TOP]

Pubmed ID :28075010
Publication Date : //
In this study, we examine whether an anti-inflammatory thiourea derivative, compound #326, actions on ion channels. The effects of compound #326 on Ca -activated K channels were evaluated by patch-clamp recordings obtained in cell-attached, inside-out or whole-cell configuration. In pituitary GH cells, compound #326 increased the amplitude of Ca -activated K currents (I ) with an EC value of 11.6 μM, which was reversed by verruculogen, but not tolbutamide or TRAM-34. Under inside-out configuration, a bath application of compound #326 raised the probability of large-conductance Ca -activated K (BK ) channels. The activation curve of BK channels was shifted to less depolarised potential with no modification of the gating charge of the curve; consequently, the difference of free energy was reduced in the presence of this compound. Compound #326-stimulated activity of BK channels is explained by a shortening of mean closed time, despite its inability to alter single-channel conductance. Neither delayed-rectifier nor erg-mediated K currents was modified. Compound #326 decreased the peak amplitude of voltage-gated Na current with no clear change in the overall current-voltage relationship of this current. In HEK293T cells expressing α-hSlo, compound #326 enhanced BK channels effectively. Intriguingly, the inhibitory actions of compound #326 on interleukin 1β in lipopolysaccharide-activated microglia were significantly reversed by verruculogen, whereas BK channel inhibitors suppressed the expressions of inducible nitric oxide synthase. The BK channels could be an important target for compound #326 if similar in vivo results occur, and the multi-functionality of BK channels in modulating microglial immunity merit further investigation.

Authors : Wu Sheng-Nan, Chern Jyh-Haur, Shen Santai, Chen Hwei-Hisen, Hsu Ying-Ting, Lee Chih-Chin, Chan Ming-Huan, Lai Ming-Chi, Shie Feng-Shiun,

(10) IK acts as an immunoregulator of inflammatory arthritis by suppressing T17 cell differentiation and macrophage activation.[TOP]

Pubmed ID :28071693
Publication Date : //
Pathogenic T helper cells (T) and macrophages have been implicated in the development of rheumatoid arthritis (RA), which can lead to severe synovial inflammation and bone destruction. A range of therapies have been widely used for RA, including specific monoclonal antibodies and chemical inhibitors against inflammatory cytokines produced by these cells. However, these have not been sufficient to meet the medical need. Here, we show that in transgenic mice expressing truncated IK (tIK) cytokine, inflammatory arthritis symptoms were ameliorated as the result of suppression of the differentiation of T1 and T17 cells and of macrophage activation. During inflammatory responses, tIK cytokine systemically regulated macrophage functions and T17 cell differentiation through inactivation of the MAPK and NF-κB pathways. Interestingly, the level of tIK cytokine was higher in synovial fluid of RA patients compared with that in osteoarthritis (OA) patients. Our observations suggest that tIK cytokine can counterbalance the induction of inflammatory cells related to RA and thus could be a new therapeutic agent for the treatment of RA.

Authors : Park Hye-Lim, Lee Sang-Myeong, Min Jun-Ki, Moon Su-Jin, Kim Inki, Kang Kyung-Won, Park Sooho, Choi SeulGi, Jung Ha-Na, Lee Dong-Hee, Nam Jae-Hwan,