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Disruption of the CCL1-CCR8 axis inhibits vascular Treg recruitment and function and promotes atherosclerosis in mice.

The CC chemokine 1 (CCL1, also called I-309 or TCA3) is a potent chemoattractant for leukocytes that plays an important role in inflammatory processes and diseases through binding to its receptor CCR8. Here, we investigated the role of the CCL1-CCR8 axis in atherosclerosis. We found increased expression of CCL1 in the aortas of atherosclerosis-prone fat-fed apolipoprotein E (Apoe)-null mice; moreover, in vitro flow chamber assays and in vivo intravital microscopy demonstrated an essential role for CCL1 in leukocyte recruitment. Mice doubly deficient for CCL1 and Apoe exhibited enhanced atherosclerosis in aorta, which was associated with reduced plasma levels of the anti-inflammatory interleukin 10, an increased splenocyte Th1/Th2 ratio, and a reduced regulatory T cell (Treg) content in aorta and spleen. Reduced Treg recruitment and aggravated atherosclerosis were also detected in the aortas of fat-fed low-density lipoprotein receptor-null mice treated with CCR8 blocking antibodies. These findings demonstrate that disruption of the CCL1-CCR8 axis promotes atherosclerosis by inhibiting interleukin 10 production and Treg recruitment and function.

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Androgen Receptor (Phosph Androgen Receptor (Phosph Rabbit Anti-Human Androge Rabbit Anti-Human Androge Androgen Receptor (Ab 650 AZD-3514 Mechanisms: Andr 17β-Acetoxy-2α-bromo-5 (5α,16β)-N-Acetyl-16-[2 (5α,16β)-N-Acetyl-16-ac 5α-N-Acetyl-2'H-androst- 5α-N-Acetyl-2'H-androst- 3-O-Acetyl 5,14-Androstad

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IL-33-induced atopic dermatitis-like inflammation in mice is mediated by group 2 innate lymphoid cells in concert with basophils.

IL-33 is a pro-inflammatory cytokine that plays a pivotal role in allergic disorders. In a transgenic mouse expressing IL-33 driven by a keratin-14 promoter (IL33tg), atopic dermatitis (AD)-like inflammation develops spontaneously with the activation of group 2 innate lymphoid cells (ILC2s). However, it remains unknown how effector cells, such as Th2 cells, ILC2s, and basophils, contribute to the inflammatory process induced by IL-33. To address the question, we examined the phenotype of IL33tg mice lacking each of these cells. Unexpectedly, AD-like inflammation still developed in Rag2KO IL33tg mice lacking T and B cells. In contrast, when ILC2s were depleted in IL33tg mice via bone marrow transplantation from ILC2-lacking, RORα-deficient mice, the development of AD-like inflammation was almost suppressed. Basophils were accumulated in the inflamed skin of IL33tg mice, and AD-like inflammation was alleviated by the conditional depletion of basophils using anti-FcεRIα antibodies or a Bas-TRECK transgenic mouse system. In these basophil-depleted IL33tg skins, ILC2s were decreased and cytokines and chemokines such as IL-5, IL-13, and CCL5 were reduced. From these results, we suggest that IL-33-induced AD-like inflammation is dependent on innate immune responses that are mediated by ILC2s in concert with basophils.

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Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Rabbit Anti-APIP Apaf1 In Rabbit Anti-APIP Apaf1 In Rabbit Anti-Cell death in Rabbit Anti-Cell death in anti-Diazepam Binding Inh anti-Diazepam Binding Inh Eosin 5 isothiocyanate, R Interleukin-34 IL34 (N-t

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E-cadherin is important for Meibomian gland function as revealed by a new human ex vivo slice culture model.

Meibomian glands within the eyelid are important for the maintenance of the integrity and health of the ocular surface. Patients with the blistering skin disease pemphigus vulgaris (PV), which is caused by autoantibodies against desmosomal cadherins, often suffer from Dry Eye Disease (DED). Therefore, we studied regulation of cell cohesion in human Meibomian gland epithelial cells (HMGEC). During serum-induced differentiation for 1d up to 6d, HMGEC drastically enhanced intercellular cohesion whereas lipid production did not change. The expression profiles of the desmosomal PV-antigens desmoglein (Dsg) 3 and 1 but not of the adherens junction component E-cadherin (Ecad) was dependent on the presence of serum. Surprisingly, after 1d but not after 6d of serum-induced differentiation, an inhibitory antibody against Ecad drastically reduced intercellular cohesion and blocked lipid production of HMGEC. In contrast, antibodies against desmosomal cadherins including human and mouse pemphigus autoantibodies had no effect on monolayer integrity and lipid production. Because in Meibomian glands from Dsg3-deficient mice lipid production was unaltered, we established an ex vivo slice culture model of human eyelids to allow studies in a more physiological environment. Here, the inhibitory antibody against Ecad but not a Dsg3-specific PV-antibody interfered with stimulated lipid production. Together, these data demonstrate that cell cohesion is maintained differently in Meibomian gland cells and indicate that E-cadherin is important for Meibomian gland function.

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Bone Morphogenetic Protei Growth Differentiation Fa NATIVE HUMAN PROLACTIN, P Active human antiplasmin Active human PAI-1 functi Active human tPA function Total Human tPA Functiona Active Human uPA Function AccuPrep Genomic DNA Extr MOUSE ANTI HUMAN CD15, Pr NATIVE HUMAN PROLACTIN, P MOUSE ANTI HUMAN CD19 RPE

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A single dose of antibody-drug conjugate cures a stage 1 model of African trypanosomiasis.

Infections of humans and livestock with African trypanosomes are treated with drugs introduced decades ago that are not always fully effective and often have severe side effects. Here, the trypanosome haptoglobin-haemoglobin receptor (HpHbR) has been exploited as a route of uptake for an antibody-drug conjugate (ADC) that is completely effective against Trypanosoma brucei in the standard mouse model of infection. Recombinant human anti-HpHbR monoclonal antibodies were isolated and shown to be internalised in a receptor-dependent manner. Antibodies were conjugated to a pyrrolobenzodiazepine (PBD) toxin and killed T. brucei in vitro at picomolar concentrations. A single therapeutic dose (0.25 mg/kg) of a HpHbR antibody-PBD conjugate completely cured a T. brucei mouse infection within 2 days with no re-emergence of infection over a subsequent time course of 77 days. These experiments provide a demonstration of how ADCs can be exploited to treat protozoal diseases that desperately require new therapeutics.

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Rabbit Anti-ACTH (7-23) P Rabbit Anti-ACTH (7-23) P Rabbit Anti-ACTH (7-23) P Rabbit Anti-ACTH (7-23) P Rabbit Anti-ACTH (7-23) P Rabbit Anti-ACTH (7-23) P Rabbit Anti-ACTH (7-23) P Rabbit Anti-ACTH (7-23) P Rabbit Anti-ACTH (7-23) P Rabbit Anti-ACTH (7-23) P Rabbit Anti-ACTH (7-23) P Rabbit Anti-ACTH (7-23) P

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Development and characterisation of novel anti-C5 monoclonal antibodies capable of inhibiting complement in multiple species.

Over the last decade there has been an explosion in complement therapies; one third of the drugs in the clinic or in development target C5 protein. Eculizumab, a monoclonal antibody (mAb) that binds C5 and blocks its cleavage by the convertase, is the current gold standard treatment for atypical haemolytic uremic syndrome (aHUS) and paroxysmal nocturnal haemoglobinuria (PNH) and in clinical trials for many other diseases. Here we describe a panel of novel anti-C5 mAb, including mAb that, like Eculizumab, are efficient inhibitors of complement but, unlike Eculizumab, inhibit across species, including human, rat, rabbit and guinea pig. Several inhibitory anti-C5 mAb were identified and characterised for C5 binding and lytic inhibitory capacity in comparison to current therapeutic anti-C5 mAb; three clones, 4G2, 7D4 and 10B6, were selected and further characterised for ligand specificity and affinity and cross-species inhibitory activity. The mAb 10B6 was human-specific while mAb 4G2 and 7D4 efficiently inhibited lysis by human, rabbit and rat serum, and weakly inhibited guinea pig complement; 7D4 also weakly inhibited mouse complement in vitro The rat C5-cross-reactive mAb 4G2, when administered intraperitoneally in a rat model of myasthenia gravis, effectively blocked the disease and protected muscle endplates from destruction. To our knowledge this is the first report of an anti-C5 function blocking mAb that permits preclinical studies in rats. This article is protected by copyright. All rights reserved.

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Goat Anti-Human Complemen Mouse monoclonal anti-fla Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse Rat monoclonal anti mouse

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GALECTIN-8 Is a Neuroprotective Factor in the Brain that Can Be Neutralized by Human Autoantibodies.

Galectin-8 (Gal-8) is a glycan-binding protein that modulates a variety of cellular processes interacting with cell surface glycoproteins. Neutralizing anti-Gal-8 antibodies that block Gal-8 functions have been described in autoimmune and inflammatory disorders, likely playing pathogenic roles. In the brain, Gal-8 is highly expressed in the choroid plexus and accordingly has been detected in human cerebrospinal fluid. It protects against central nervous system autoimmune damage through its immune-suppressive potential. Whether Gal-8 plays a direct role upon neurons remains unknown. Here, we show that Gal-8 protects hippocampal neurons in primary culture against damaging conditions such as nutrient deprivation, glutamate-induced excitotoxicity, hydrogen peroxide (HO)-induced oxidative stress, and β-amyloid oligomers (Aβo). This protective action is manifested even after 2 h of exposure to the harmful condition. Pull-down assays demonstrate binding of Gal-8 to selected β1-integrins, including α3 and α5β1. Furthermore, Gal-8 activates β1-integrins, ERK1/2, and PI3K/AKT signaling pathways that mediate neuroprotection. Hippocampal neurons in primary culture produce and secrete Gal-8, and their survival decreases upon incubation with human function-blocking Gal-8 autoantibodies obtained from lupus patients. Despite the low levels of Gal-8 expression detected by real-time PCR in hippocampus, compared with other brain regions, the complete lack of Gal-8 in Gal-8 KO mice determines higher levels of apoptosis upon HO stereotaxic injection in this region. Therefore, endogenous Gal-8 likely contributes to generate a neuroprotective environment in the brain, which might be eventually counteracted by human function-blocking autoantibodies.

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TGF beta induced factor 2 Beta Amyloid (42) ELISA K Beta Amyloid (1 40) ELISA Beta Amyloid (40) ELISA K Beta Amyloid (1 40) ELISA Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Goat Anti-Human Laforin ( Mouse Anti-Human Interleu Mouse Anti-Human Interleu Mouse Anti-Human Interleu interleukin 17 receptor C

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Recombinant lactococcus lactis secreting viral protein 1 of enterovirus 71 and its immunogenicity in mice.

To construct recombinant Lactococcus lactis (L. lactis) expressing viral protein 1 (VP1) of enterovirus 71 (EV71) and evaluate its immunogenicity to be used as an oral vaccine in BALB/c mice.

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Recombinant HIV-1 pol Int Recombinant HIV-1 p31 Int Recombinant Influenza HA Recombinant Influenza HA Recombinant Influenza HA Recombinant Rubella Viral Recombinant Influenza (H5 Recombinant Influenza (H5 Recombinant Influenza (H5 Viral antibodies, anti-H Recombinant Human Androge Recombinant Viral Antige

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Immunotherapy of Endothelin-1 Receptor Type A for Pulmonary Arterial Hypertension.

Pulmonary arterial hypertension (PAH) is a chronic fatal disease. The treatment of PAH is less than ideal and the control is far from satisfactory worldwide. Vaccination provides a promising approach for treatment of PAH.

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Novel anti-CD38 humanized mAb SG003 possessed enhanced cytotoxicity in lymphoma than Daratumumab via antibody-dependent cell-mediated cytotoxicity.

In vivo use of monoclonal antibodies has become routine clinical practice in the treatment of human cancer. CD38 is an attractive target, because it has double roles, as a receptor and an ectoenzyme. Daratumumab, an anti-CD38 antibody, is currently in the clinical trials for multiple myeloma.

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Monoclonal Antibody Detection of Porcine Meat.

A stable hybridoma cell line (DD9) has been produced secreting a monoclonal antibody specific for porcine muscle proteins. The DD9 monoclonal antibody (mAb) failed to show a significant cross-reactivity when tested against beef, horse, chicken, and soya proteins, as well as bovine caseins, gelatin, and bovine serum albumin. The DD9 mAb was further used in an indirect ELISA format for detection of defined amounts of porcine meat (1-100%) in beef and chicken meat mixtures immobilized on 96-well plates. Immunorecognition of monoclonal antibodies adsorbed to porcine meat was made with rabbit anti-mouse immunoglobulins conjugated to the enzyme horseradish peroxidase.

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Anti C Reactive Protein A MOUSE ANTI BOVINE ROTAVIR Detection Buffer A&B Anti Detection Buffer C&D Anti Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Mouse, Monoclon Anti AGO2 Human, Monoclon Anti AGO2 Human, Monoclon

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