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Search results for: Anti annexin A1 Monoclonal

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#32533866   2020/07/09 To Up

Monoclonal antibody therapy that targets phospholipid-binding protein delays lupus activity in MRL/lpr mice.

Systemic lupus erythematosus is an autoimmune syndrome characterized by the development of autoantibodies to a wide range of antigens. Together with B cells, respective self-reactive T cells have an important contribution in disease progression as being responsible for inflammatory cytokines secretion, B cell activation and promoting amplification of the autoimmune response. Annexin A1 is expressed by many cell types and binds to phospholipids in a Ca -dependent manner. Abnormal expression of annexin A1 was found on activated B and T cells in both murine and human autoimmunity suggesting its potential role as a therapeutic target. In the present study, we have investigated the possibility to suppress autoimmune manifestation in spontaneous mouse model of lupus using anti-annexin A1 antibody. Groups of lupus-prone MRL/lpr mice were treated with the anti-annexin A1 monoclonal antibody, and the disease activity and survival of the animals were following up. Flow cytometry, ELISA assays, and histological and immunofluorescence kidney analyses were used to determine the levels of Annexin A1 expression, cytokines, anti-dsDNA antibodies and kidney injuries. The administration of this monoclonal antibody to MRL/lpr mice resulted in suppression of IgG anti-dsDNA antibody production, modulated IL-10 secretion, decreased disease activity and prolonged survival compared with the control group.
Nikolina Mihaylova, Silviya Bradyanova, Petroslav Chipinski, Stela Chausheva, Dobroslav Kyurkchiev, Andrey I Tchorbanov

1729 related Products with: Monoclonal antibody therapy that targets phospholipid-binding protein delays lupus activity in MRL/lpr mice.

100.00 ug100.00 ug100.00 ug1mg100100.00 ug100100ul100.00 ug1001 Set1 Set

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#29738458   2018/05/08 To Up

The Annexin A1 Receptor FPR2 Regulates the Endosomal Export of Influenza Virus.

The Formyl Peptide Receptor 2 (FPR2) is a novel promising target for the treatment of influenza. During viral infection, FPR2 is activated by annexinA1, which is present in the envelope of influenza viruses; this activation promotes virus replication. Here, we investigated whether blockage of FPR2 would affect the genome trafficking of influenza virus. We found that, upon infection and cell treatment with the specific FPR2 antagonist WRW4 or the anti-FPR2 monoclonal antibody, FN-1D6-AI, influenza viruses were blocked into endosomes. This effect was independent on the strain and was observed for H1N1 and H3N2 viruses. In addition, blocking FPR2signaling in alveolar lung A549 epithelial cells with the monoclonal anti-FPR2 antibody significantly inhibited virus replication. Altogether, these results show that FPR2signaling interferes with the endosomal trafficking of influenza viruses and provides, for the first time, the proof of concept that monoclonal antibodies directed against FPR2 inhibit virus replication. Antibodies-based therapeutics have emerged as attractive reagents in infectious diseases. Thus, this study suggests that the use of anti-FPR2 antibodies against influenza hold great promise for the future.
Fryad Rahman, Mohammad Chebbo, Noémie Courtin, Aurelien Fotso Fotso, Marie-Christine Alessi, Béatrice Riteau

1383 related Products with: The Annexin A1 Receptor FPR2 Regulates the Endosomal Export of Influenza Virus.

1 mg101 mL10 500 10011 mg0.1 mg

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#28300427   2017/03/16 To Up

Annexin A1 as a target for managing murine pristane-induced systemic lupus erythematosus.

Systemic lupus erythematosus (SLE) is a polygenic pathological disorder which involves multiple organs. Self-specific B cells play a main role in the lupus pathogenesis by generating autoantibodies as well as by serving as important autoantigen-presenting cells. Autoreactive T lymphocytes, on the other hand, are responsible for B cell activation and proliferation, and cytokine production. Therefore, both factors promote the idea that a down-modulation of activated self-reactive T and B cells involved in the pathogenic immune response is a reasonable approach for SLE therapy. Annexin A1 (ANX A1) is expressed by many cell types and binds to phospholipids in a Ca dependent manner. Abnormal expression of ANX A1 was found on activated B and T cells in both murine and human autoimmunity, suggesting its potential role as a therapeutic target. While its role on T lymphocytes is through formyl peptide receptor-like molecules (FPRL), and the formed ANX A1/FPRL pathway modulates T cell receptor signalling, there is still no fool-proof data available for the role of ANX A1 in B cells. We employed a lupus model of Balb/c mice with pristane-induced SLE which very closely resembles human lupus. In the present study, we investigated the possibility to modulate the autoimmune response in a pristane-induced mouse model of SLE using an anti- ANX A1 antibody. Administration of this monoclonal antibody resulted in the inhibition of T-cell activation and proliferation, suppression of IgG anti-dsDNA antibody-secreting plasma cells and of proteinuria, decreased disease activity and prolonged survival compared to control group.
Nikolina Mihaylova, Silviya Bradyanova, Petroslav Chipinski, Melinda Herbáth, Stela Chausheva, Dobroslav Kyurkchiev, József Prechl, Andrey I Tchorbanov

1951 related Products with: Annexin A1 as a target for managing murine pristane-induced systemic lupus erythematosus.

250 ml100Tests100 assays0.1ml (1mg/ml)1 mg25 µg0.2 mg200 assays1 mg (4000 assays)400 assays1 kit

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#26902275   // To Up

[Changes in the expression of three markers in T lymphocytes of peripheral blood and immunoregulatory mechanisms of burned mice with sepsis at early stage].

To study the expression levels of annexin A1 (ANXA1), GATA-3, and T-bet in T lymphocytes of peripheral blood in burned mice with sepsis at early stage, and to analyze their immune regulatory mechanisms.
Yuxiang Zhou, Peng Huang, Pihong Zhang, Licheng Ren, Jizhang Zeng, Jie Zhou, Pengfei Liang, Xiaoyuan Huang

1536 related Products with: [Changes in the expression of three markers in T lymphocytes of peripheral blood and immunoregulatory mechanisms of burned mice with sepsis at early stage].



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#24130820   2013/10/10 To Up

Dysregulation of anti-inflammatory annexin A1 expression in progressive Crohns Disease.

Development of inflammatory bowel disease (IBD) involves the interplay of environmental and genetic factors with the host immune system. Mechanisms contributing to immune dysregulation in IBD are not fully defined. Development of novel therapeutic strategies is focused on controlling aberrant immune response in IBD. Current IBD therapy utilizes a combination of immunomodulators and biologics to suppress pro-inflammatory effectors of IBD. However, the role of immunomodulatory factors such as annexin A1 (ANXA1) is not well understood. The goal of this study was to examine the association between ANXA1 and IBD, and the effects of anti-TNF-α, Infliximab (IFX), therapy on ANXA1 expression.
Angela Sena, Irina Grishina, Anne Thai, Larissa Goulart, Monica Macal, Anne Fenton, Jay Li, Thomas Prindiville, Sonia Maria Oliani, Satya Dandekar, Luiz Goulart, Sumathi Sankaran-Walters

1441 related Products with: Dysregulation of anti-inflammatory annexin A1 expression in progressive Crohns Disease.

50 UG100 μg100 μg100 μg100 μg100ug Lyophilized100 100ug Lyophilized

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#23527056   2013/03/18 To Up

Anti-allergic cromones inhibit histamine and eicosanoid release from activated human and murine mast cells by releasing Annexin A1.

Although the 'cromones' (di-sodium cromoglycate and sodium nedocromil) are used to treat allergy and asthma, their 'mast cell stabilising' mechanism of pharmacological action has never been convincingly explained. Here, we investigate the hypothesis that these drugs act by stimulating the release of the anti-inflammatory protein Annexin-A1 (Anx-A1) from mast cells.
Samia Yazid, Ajantha Sinniah, Egle Solito, Virginia Calder, Rod J Flower

1009 related Products with: Anti-allergic cromones inhibit histamine and eicosanoid release from activated human and murine mast cells by releasing Annexin A1.

0.1 mg200 1 mg1 ml1000 100 ug/vial100μg100 200 50 mg25 100 ug/vial

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#23475487   2013/03/01 To Up

Mechanisms of action of the anti-VEGF monoclonal antibody bevacizumab on chronic lymphocytic leukemia cells.

Chronic lymphocytic leukemia (CLL) remains incurable; therefore searching for new therapeutic strategies in this disease is necessary. An important mechanism of tumor development is neoangiogenesis. A potent antiangiogenic factor, bevacizumab (Avastin, AVA), has been poorly explored in CLL so far. In the current study we assessed cytotoxic activity of AVA alone or in combinations with drugs routinely used in this disease.
Jakub Bogusz, Agata Majchrzak, Aleksandra Mędra, Barbara Cebula-Obrzut, Tadeusz Robak, Piotr Smolewski

1905 related Products with: Mechanisms of action of the anti-VEGF monoclonal antibody bevacizumab on chronic lymphocytic leukemia cells.

100ul100ul100ul100ul 50 UG100ul1mg100ug Lyophilized0.25100ul25 µg 50UG

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#21176713   // To Up

Annexin-1 is no useful surrogate marker of multiple sclerosis - an immunocytochemical study of the cerebrospinal fluid.

Annexin-1 is a calcium-binding protein with anti-inflammatory properties, which has previously been described in MS plaque tissue. We investigated the feasibility and specificity of annexin-1-immuncytochemistry of CSF cells to test its potential as a surrogate marker for MS.
S Probst-Cousin, D Heuss, M Bergmann

1587 related Products with: Annexin-1 is no useful surrogate marker of multiple sclerosis - an immunocytochemical study of the cerebrospinal fluid.

100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized100ug Lyophilized

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