Search results for: Leukotriene B4 Receptor(BLT1 Receptor) Antibody
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#31943941 2020/04/26 To Up
Requirement of Mucosa-Associated Lymphoid Tissue Lymphoma Translocation Protein 1 Protease Activity for FcÎ³ Receptor-Induced Arthritis, but Not FcÎ³ Receptor-Mediated Platelet Elimination, in Mice.FcÎ³ receptors (FcÎ³R) play important roles in both protective and pathogenic immune responses. The assembly of the CBM signalosome encompassing caspase recruitment domain-containing protein 9, B cell CLL/lymphoma 10, and mucosa-associated lymphoid tissue lymphoma translocation protein 1 (MALT-1) is required for optimal FcÎ³R-induced canonical NF-ÎºB activation and proinflammatory cytokine release. This study was undertaken to clarify the relevance of MALT-1 protease activity in FcÎ³R-driven events and evaluate the therapeutic potential of selective MALT-1 protease inhibitors in FcÎ³R-mediated diseases.
Kea Martin, Ratiba Touil, Grozdan Cvijetic, Laura Israel, Yeter Kolb, Sophie Sarret, StÃ©phanie Valeaux, Elena Degl'Innocenti, Thomas Le Meur, Nadja Caesar, Maureen Bardet, Christian Beerli, Hans-Guenter Zerwes, Jiri Kovarik, Karen Beltz, Achim Schlapbach, Jean Quancard, Catherine H RÃ©gnier, Marc Bigaud, Tobias Junt, Grazyna Wieczorek, Isabelle Isnardi, Amanda Littlewood-Evans, FrÃ©dÃ©ric Bornancin, Thomas Calzascia
1036 related Products with: Requirement of Mucosa-Associated Lymphoid Tissue Lymphoma Translocation Protein 1 Protease Activity for FcÎ³ Receptor-Induced Arthritis, but Not FcÎ³ Receptor-Mediated Platelet Elimination, in Mice.200ul100ug Lyophilized 100ul100ug Lyophilized100ug Lyophilized100ug100ug100ug100ug100ug100ug100ug
#30659825 2019/01/16 To Up
Î²2-Microglobulin, interleukin-31, and arachidonic acid metabolites (leukotriene B and thromboxane A) are involved in chronic renal failure-associated itch-associated responses in mice.Chronic renal failure (CRF) is a progressive disease with severe pruritus and dry skin as the major symptoms. However, the mechanisms of CRF-induced pruritus remain unclear. In this study, 5/6 nephrectomized (NPCT) mice were used as a mouse model of CRF. Serum concentrations of blood urea nitrogen and creatinine in 5/6 NPCT mice were increased. The stratum corneum water content in the skin of 5/6 NPCT mice was decreased. These findings suggest that 5/6 nephrectomy in mice results in a phenotype resembling human CRF. 5/6 NPCT mice showed spontaneous scratching, which was inhibited by Î¼-opioid receptor antagonist, suggesting that the scratching is an itch-related response. The number of cutaneous mast cells was not altered in 5/6 NPCT mice compared with sham-operated mice. The H histamine-receptor antagonist, proteinase-activated receptor 2-neutralizing antibody, and 5-HT-receptor antagonist did not inhibit spontaneous scratching in 5/6 NPCT mice; therefore, the role of mast cells and serotonin in spontaneous scratching appears to be minimal. The anti-allergy agent azelastine, BLT leukotriene (LT) B receptor antagonist, and TP thromboxane (TX) A receptor antagonist inhibited spontaneous scratching in 5/6 NPCT mice, suggesting that LTB and TXA are involved in CRF-induced pruritus. Interestingly, in the skin of 5/6 NPCT mice, levels of two newly identified pruritogens (Î²2-microglobulin and interleukin-31) were increased. Taken together, these findings suggest that 5/6 NPCT mice are useful for the study of itching in CRF. In addition to LTB and TXA, it is also suggested that Î²2-microglobulin and interleukin-31 are involved in itching associated with CRF-induced pruritus.
Sikai Li, Tsugunobu Andoh, Qun Zhang, Daisuke Uta, Yasushi Kuraishi
1286 related Products with: Î²2-Microglobulin, interleukin-31, and arachidonic acid metabolites (leukotriene B and thromboxane A) are involved in chronic renal failure-associated itch-associated responses in mice.50 UG25 mg2 1 mg10 mg25 mg12ug96tests96 wells (1 kit)10 mg
#30019426 2018/08/14 To Up
Development of psoriasis by continuous neutrophil infiltration into the epidermis.Remarkable effects of anti-IL-17A and anti-IL-23 antibodies on psoriasis indicate deep involvement of IL-23/Th17 axis in the pathogenesis of psoriasis. According to the current immune theory, activation of dendritic cells initiates the generation of this axis. However, this theory is not enough to explain the mechanism, because the process of this activation is obscure and the antigen that is recognized by antigen-presenting cells and pathogenic T cells has long been unidentified. Therefore, I thought of another theory as follows. Neutrophils are attracted by LTB4 at subcorneal portion and infiltrate into the epidermis. At the time of neutrophil migration through the basement membrane, basal keratinocytes in G0/G1 phase enter the cell cycle and begin to proliferate, according to the principle, "detachment-mediated cell proliferation." This passing is continuously repeated and leads to elongation of rete ridges. The IL-23/Th17 axis is generated by interactions between infiltrated neutrophils and keratinocytes. Briefly, neutrophils infiltrated into the epidermis secrete IL-17A, which acts on keratinocytes to express CCL20, a ligand for the chemokine receptor CCR6. Keratinocytes perturbed by neutrophil infiltration produce HSP70, followed by production of IL-23 via TLR4 using HSP70 as an endogenous ligand for TLR4. Natural Th17 cells expressing CCR6 are recruited to psoriatic epidermis and expand there in the presence of IL-23 and IL-1Î². In this manner, the framework of the IL-23/Th17 axis is created, which acts to maintain or exacerbate psoriasis. Noteworthy is the fact that this axis causes positive feedback loop, starting from IL-17A production by neutrophils and ending in IL-17A production by nTh17 cells. Therapeutic mechanisms of anti-IL-17A and anti-IL-23 antibodies, targeting neutrophils, were also described.
2806 related Products with: Development of psoriasis by continuous neutrophil infiltration into the epidermis.300 units100ug Lyophilized500 Units25 1500 pcs100ug Lyophilized10
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#28922396 2017/09/18 To Up
Biochemical and immunological characterization of a novel monoclonal antibody against mouse leukotriene B4 receptor 1.Leukotriene B4 (LTB4) receptor 1 (BLT1) is a G protein-coupled receptor expressed in various leukocyte subsets; however, the precise expression of mouse BLT1 (mBLT1) has not been reported because a mBLT1 monoclonal antibody (mAb) has not been available. In this study, we present the successful establishment of a hybridoma cell line (clone 7A8) that produces a high-affinity mAb for mBLT1 by direct immunization of BLT1-deficient mice with mBLT1-overexpressing cells. The specificity of clone 7A8 was confirmed using mBLT1-overexpressing cells and mouse peripheral blood leukocytes that endogenously express BLT1. Clone 7A8 did not cross-react with human BLT1 or other G protein-coupled receptors, including human chemokine (C-X-C motif) receptor 4. The 7A8 mAb binds to the second extracellular loop of mBLT1 and did not affect LTB4 binding or intracellular calcium mobilization by LTB4. The 7A8 mAb positively stained Gr-1-positive granulocytes, CD11b-positive granulocytes/monocytes, F4/80-positive monocytes, CCR2-high and CCR2-low monocyte subsets in the peripheral blood and a CD4-positive T cell subset, Th1 cells differentiated in vitro from naÃ¯ve CD4-positive T cells. This mAb was able to detect Gr-1-positive granulocytes and monocytes in the spleens of naÃ¯ve mice by immunohistochemistry. Finally, intraperitoneal administration of 7A8 mAb depleted granulocytes and monocytes in the peripheral blood. We have therefore succeeded in generating a high-affinity anti-mBLT1 mAb that is useful for analyzing mBLT1 expression in vitro and in vivo.
Fumiyuki Sasaki, Tomoaki Koga, Kazuko Saeki, Toshiaki Okuno, Saiko Kazuno, Tsutomu Fujimura, Yasuyuki Ohkawa, Takehiko Yokomizo
1893 related Products with: Biochemical and immunological characterization of a novel monoclonal antibody against mouse leukotriene B4 receptor 1.0.1 mg100ul100ul100ul100ug1 mg100 ug50 ug 100 ug100 ug100 ug200 ug
#28736835 2017/09/06 To Up
Peptide mimetics of immunoglobulin A (IgA) and FcÎ±RI block IgA-induced human neutrophil activation and migration.The cross-linking of the IgA Fc receptor (FcÎ±RI) by IgA induces release of the chemoattractant LTB4, thereby recruiting neutrophils in a positive feedback loop. IgA autoantibodies of patients with autoimmune blistering skin diseases therefore induce massive recruitment of neutrophils, resulting in severe tissue damage. To interfere with neutrophil mobilization and reduce disease morbidity, we developed a panel of specific peptides mimicking either IgA or FcÎ±RI sequences. CLIPS technology was used to stabilize three-dimensional structures and to increase peptides' half-life. IgA and FcÎ±RI peptides reduced phagocytosis of IgA-coated beads, as well as IgA-induced ROS production and neutrophil migration in in vitro and ex vivo (human skin) experiments. Since topical application would be the preferential route of administration, Cetomacrogol cream containing an IgA CLIPS peptide was developed. In the presence of a skin permeation enhancer, peptides in this cream were shown to penetrate the skin, while not diffusing systemically. Finally, epitope mapping was used to discover sequences important for binding between IgA and FcÎ±RI. In conclusion, a cream containing IgA or FcÎ±RI peptide mimetics, which block IgA-induced neutrophil activation and migration in the skin may have therapeutic potential for patients with IgA-mediated blistering skin diseases.
Marieke H Heineke, Lydia P E van der Steen, Rianne M Korthouwer, J Joris Hage, Johannes P M Langedijk, Joris J Benschop, Jantine E Bakema, Jerry W Slootstra, Marjolein van Egmond
1996 related Products with: Peptide mimetics of immunoglobulin A (IgA) and FcÎ±RI block IgA-induced human neutrophil activation and migration.50 ul100 ul0.1 mg100ul1 ml200 1000 5 G50 ug50 ug0.1 mg
#28108297 2017/01/17 To Up
The Leukotriene B and its Receptor BLT1Â ActÂ as Critical Drivers of Neutrophil Recruitment in Murine Bullous Pemphigoid-Like Epidermolysis Bullosa Acquisita.Recruitment of neutrophils and eosinophils into the skin is a hallmark of pemphigoid diseases. The molecular cues regulating granulocyte recruitment into the skin and the individual contributions of neutrophils and eosinophils to pemphigoid diseases are, however, poorly understood. The lipid mediator leukotriene B (LTB) is a potent granulocyte chemoattractant and is abundant in the skin blister fluid of bullous pemphigoid (BP) patients, but its pathogenic significance is unknown. Using mouse models of BP-like epidermolysis bullosa acquisita and of BP, we show that LTB and its receptor BLT1 act as critical drivers of neutrophil entry into the skin upon antibody deposition at the dermal-epidermal junction. Mice deficient in 5-lipoxygenase, a key enzyme in LTB biosynthesis, or in BLT1 exhibited dramatic resistance to neutrophil recruitment and, consequently, skin inflammation. Accordingly, liquid chromatography-mass spectrometry, used to comprehensively profile lipid mediator generation in the first 48 hours after antibody deposition, showed a pronounced parallel increase in LTB and in neutrophils in the skin. Subsequent mechanistic studies in BP-like epidermolysis bullosa acquisita uncovered that neutrophils are necessary for skin inflammation, whereas eosinophils are dispensable, thus identifying neutrophils as major culprits of blister formation. Our results highlight LTB/BLT1 as absolutely critical drivers of murine pemphigoid disease-like skin inflammation.
Tanya Sezin, Matthias Krajewski, Adam Wutkowski, Sadegh Mousavi, Lenche Chakievska, Katja Bieber, Ralf J Ludwig, Markus Dahlke, Dirk Rades, Franziska S Schulze, Enno Schmidt, Kathrin Kalies, Yask Gupta, Paul Schilf, Saleh M Ibrahim, Peter KÃ¶nig, Dominik Schwudke, Detlef Zillikens, Christian D Sadik
1285 related Products with: The Leukotriene B and its Receptor BLT1Â ActÂ as Critical Drivers of Neutrophil Recruitment in Murine Bullous Pemphigoid-Like Epidermolysis Bullosa Acquisita.100ug100ug100ug Lyophilized196 wells (1 kit)100ug100ug Lyophilized100 assays48 assays100ug
#27730145 2015/12/22 To Up
Trans-basement membrane migration of eosinophils induced by LPS-stimulated neutrophils from human peripheral blood .In the airways of severe asthmatics, an increase of neutrophils and eosinophils is often observed despite high-dose corticosteroid therapy. We previously reported that interleukin-8-stimulated neutrophils induced trans-basement membrane migration (TBM) of eosinophils, suggesting the link between neutrophils and eosinophils. Concentrations of lipopolysaccharide (LPS) in the airway increase in severe asthma. As neutrophils express Toll-like receptor (TLR)4 and can release chemoattractants for eosinophils, we investigated whether LPS-stimulated neutrophils modify eosinophil TBM. Neutrophils and eosinophils were isolated from peripheral blood of healthy volunteers and severe asthmatics. Eosinophil TBM was examined using a modified Boyden's chamber technique. Eosinophils were added to the upper compartment, and neutrophils and LPS were added to the lower compartment. Migrated eosinophils were measured by eosinophil peroxidase assays. LPS-stimulated neutrophils induced eosinophil TBM (about 10-fold increase), although LPS or neutrophils alone did not. A leukotriene B receptor antagonist, a platelet-activating factor receptor antagonist or an anti-TLR4 antibody decreased eosinophil TBM enhanced by LPS-stimulated neutrophils by almost half. Neutrophils from severe asthmatics induced eosinophil TBM and lower concentrations of LPS augmented neutrophil-induced eosinophil TBM. These results suggest that the combination of neutrophils and LPS leads eosinophils to accumulate in the airways, possibly involved the pathogenesis of severe asthma.
Fuyumi Nishihara, Kazuyuki Nakagome, Takehito Kobayashi, Toru Noguchi, Ryuichiro Araki, Yoshitaka Uchida, Tomoyuki Soma, Makoto Nagata
2026 related Products with: Trans-basement membrane migration of eosinophils induced by LPS-stimulated neutrophils from human peripheral blood .100 UG100 ul4 Membranes/Box5ug 100ul1ml4 Membranes/Box4 Membranes/Box 100ul4 Membranes/Box 1 kit(s) 1 mg
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