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发布于:2019-5-16 23:00:39  访问:15 次 回复:0 篇
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Ingly, CD4 down-modulation was observed in BT-061 treated synovial fluid punctuated
3Biostatistics, Helmholtz Centre for Infection Study, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/23907221 Inhoffenstra 7, D38124 Braunschweig, Germany. 4Department of Immunology Genetics and Pathology, Uppsala University, Rudbeck Laboratory, S75185 Uppsala, Sweden. 5Immuneed AB, S-756 52, Uppsala, Sweden. 6Institute for Anatomy, University Leipzig, Liebigstra 13, D04103 Leipzig. 7Clinic for Immunology and Rheumatology, Hannover Medical School, Indole-3-carboxylic acidEpigenetic Reader Domain Carl-Neuberg-Stra 1, D30625 Hannover, Germany. 8Department of Otolaryngology, Hannover Medical College, Carl-Neuberg-Stra 1, D30625 Hannover, Germany. 9Institute for Molecular and Clinical Immunology, Medical Faculty, Otto-von-Guericke University, D39120 Magdeburg, Germany. ten Division of Immune Handle, Helmholtz Centre for Infection Research, Inhoffenstr? 7, D38124 Braunschweig, Germany. 11Biotest AG, Dreieich, Landsteinerstrasse 5, D63303 Dreieich, Germany. *These authors contributed equally to this function.Present address: Institute for Food Toxicology and Analytical Chemistry, University of Veterinary Medicine Hannover, Bischofsholer Damm 15, D30173 Hannover, Germany. Present address: Biosimilars BoehringerIngelheim, Binger Stra 73, D55218 Ingelheim am Rhein, Germany. Correspondence and requests for supplies need to be addressed to U.K. (e mail: ulrich.kalinke@twincore.de)Received: 12 August 2015.Ingly, CD4 down-modulation was observed in BT-061 treated synovial fluid punctuated from patients‘ inflamed joints that comprised enhanced numbers of CD64+ cells. In contrast, inside a circulating whole blood system injection of BT-061 did not induce CD4 down-modulation, because of CD64 saturation by serum IgG. Similarly, tonsil derived mononuclear cells devoid of CD64+ cells did not show CD4 down-modulation, whereas addition of blood derived monocytes restored the impact. As a result, the interaction of BT-061 decorated T cells with CD64+ cells is necessary for CD4 down-modulation, implying that in individuals BT061 would mostly induce CD4 down-modulation at inflammatory web-sites. These results highlight the require not only to examine the interaction of a given mAb with single FcR, but additionally the immunological atmosphere that is definitely suitable to support such interactions. Currently, a entire variety of different monoclonal antibodies (mAbs) is becoming developed for the therapy of diverse diseases, like cancer and autoimmune situations. mAb function largely is conferred by (i) depletion of target cells, (ii) inhibition of cell-cell or cell-ligand interactions, or (iii) agonistically triggering signals that impact cell function, e.g. to suppress activity of self-reactive T cells. Protein engineering gives the possibility to tailor mAb formats for provided therapeutic purposes1. Nevertheless, to become able to totally exploit such technologies, a detailed understanding of the mAb effector function is required2. Within the past, selection PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/21311040 of the continuous region (C area) for therapeutic mAbs was according to information retrieved from in vitro evaluation of effector functions for example phagocytosis, induction of inflammatory cytokines or chemokines, and antibody-dependent cellular cytoxicity (ADCC). These effectorInstitute for Experimental Infection Analysis, TWINCORE, Centre for Experimental and Clinical Infection Research, a joint venture in between the Helmholtz Centre for Infection Study (HZI) as well as the Hannover Health-related School (MHH), Feodor-Lynen-Stra 7, D30625 Hannover. 2Department of Computer Science, Ostfalia University of Applied Sciences, Salzdahlumer Stra 46/48, D38302 Wolfenb tel, Germany. 3Biostatistics, Helmholtz Centre for Infection Analysis, PubMed ID:https://www.ncbi.nlm.nih.gov/pubmed/23907221 Inhoffenstra 7, D38124 Braunschweig, Germany. 4Department of Immunology Genetics and Pathology, Uppsala University, Rudbeck Laboratory, S75185 Uppsala, Sweden.
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