Polyclonal activation of primed rat B cells |
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| Authors: | D L Burg T L Feldbush |
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| Affiliation: | 1. Curtin Health Innovation Research Institute, Curtin University, Belmont, Western Australia, Australia;2. Division of Cancer Biology, School of Biomedical Sciences, The University of Western Australia, 35 Stirling Hwy, Nedlands 6009 Western Australia, Australia;3. Perron Institute for Neurological and Translational Science, Sarich Neuroscience Research Institute Building, 8 Verdun St, Nedlands 6009 Western Australia, Australia;1. Institut de Recerca contra la Leucèmia Josep Carreras, Spain;2. Thermo Fisher Scientific, Eugene, OR, USA;1. Department of Immunology, Allergology, Rheumatology, Faculty of Medicine and Health Sciences, Antwerp, Belgium;2. Infla-Med Centre of Excellence, Antwerp University, Antwerp, Belgium;3. Immunology, Allergology, Rheumatology, Antwerp University Hospital, Antwerp, Belgium;4. Department of Immunology and Allergology, AZ Jan Palfijn Gent, Ghent, Belgium;1. Toxicology Branch, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA;2. Cardiopulmonary and Immunotoxicology Branch, National Health and Environmental Effects Research Laboratory, U.S. Environmental Protection Agency, Research Triangle Park, NC, USA;3. Office of Health Assessment and Translation, Division of the National Toxicology Program, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park, NC, USA;4. Centre for Health Protection, National Institute for Public Health and the Environment (RIVM), Bilthoven, The Netherlands;5. Department of Toxicogenomics, Maastricht University, Maastricht, The Netherlands;1. School of Architecture, Tianjin University, China;2. Institute for Environmental Design and Engineering, University College London, UK |
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| Abstract: | In recent years, murine and human virgin B lymphocytes have been used to examine the steps necessary for polyclonal activation. In these models mitogens are used in conjunction with lymphokines to determine which signals are responsible for regulating B-cell triggering, proliferation, and differentiation. While progress has been made in understanding these events as they occur in virgin B cells, very little evidence exists to suggest whether these models of activation also apply to the memory B-cell population. In this report we have described an antigen-specific, secondary in vitro immune response using cells isolated from lymph nodes draining the site of antigen injection. Unfractionated cells, B cells, and size-fractionated cells from dinitrophenyl-keyhole limpet hemocyanin (DNP-KLH)-primed rats were challenged in vitro with DNP-KLH, lipopolysaccharide plus dextran sulfate (LPS/DxS), and T-cell factors. We have consistently found, under all these conditions, that antigen challenge of primed cells results in the production of DNP-specific IgG antibody while stimulation with LPS/DxS plus T-cell factors results only in the polyclonal activation of virgin B cells; no antigen-specific IgG secretion is seen. This suggests that acquisition of memory status is associated with a loss in responsiveness to LPS/DxS-induced differentiation. |
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