Repair of Immunoglobulin Response in B Cell Line (JK32.1) Originating from Immunodeficient Patient via Implantation of Functional Plasma Membranes |
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| Institution: | 1. Department of Immunology and Infectious Disease, John Curtin School of Medical Research, The Australian National University, Canberra, ACT 2601, Australia;2. KEMRI - Wellcome Research Programme/Centre for Geographical Medicine Research (Coast), Kilifi, Kenya;3. Vaccine Research Center, National Institutes of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD 20892, USA;4. Centre for Tropical Medicine and Global Health, Nuffield Department of Medicine, University of Oxford, Oxford OX3 7FZ, UK;5. Department of Microbiology and Immunology, Peter Doherty Institute, University of Melbourne, Melbourne, VIC 3000, Australia;6. Australian Cancer Research Foundation Biomolecular Resource Facility, John Curtin School of Medical Research, The Australian National University, Canberra, ACT 2601, Australia;7. School of Medical Science, Kirby Institute, University of New South Wales, Sydney, NSW 2052, Australia;8. Center for Vaccine Development and Global Health, University of Maryland School of Medicine, Baltimore, MD 21201, USA;9. Sanaria Inc., Rockville, MD 20850, USA;10. ARC Centre of Excellence in Convergent Bio-Nano Science and Technology, The University of Melbourne, Melbourne, VIC, Australia;1. Department of Microbiology, Immunology and Molecular Genetics, Long School of Medicine, The University of Texas Health Science Center at San Antonio, San Antonio, TX 78229, USA;2. Centers for Cancer Immunotherapy and Autoimmunity, La Jolla Institute for Immunology, La Jolla, CA 92037, USA;3. Infectious Disease Research Collaboration, Kampala, Uganda;4. Department of Infection Biology, London School of Hygiene and Tropical Medicine, London WC1E 7HT, UK;5. Department of Medicine, Division of Infectious Diseases, Stanford University, Stanford, CA 94305, USA;6. Department of Microbiology and Immunology, Stanford University, Stanford, CA 94305, USA;7. Department of Medicine, University of California, San Francisco, San Francisco, CA 94110, USA;8. Department of Pediatrics, University of California, San Francisco, San Francisco, CA 94110, USA;9. Department of Pediatrics, University of California San Diego, La Jolla, CA 92093, USA;1. Department of Immunopathology, Sanquin Research and Landsteiner Laboratory, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands;2. Amsterdam Institute for Infection and Immunity, Amsterdam, The Netherlands;3. Department of Medical Microbiology and Infection Prevention, Laboratory of Experimental Virology, Amsterdam UMC, University of Amsterdam, Amsterdam, The Netherlands;4. Application Department, Cytek Biosciences Inc, Fremont, Calif;5. Department of Molecular Cell Biology and Immunology, Amsterdam Infection & Immunity and Cancer Center Amsterdam, Amsterdam University Medical Centers, Free University of Amsterdam, Amsterdam, The Netherlands;6. Department of Neurology and Neurophysiology, Amsterdam Neuroscience, University of Amsterdam, Amsterdam, The Netherlands;7. Department of Clinical Neurophysiology, St Antonius Hospital, Nieuwegein, The Netherlands;8. Department of Pediatric Immunology, Rheumatology and Infectious Diseases, Emma Children’s Hospital, Amsterdam University Medical Centers, University of Amsterdam, Amsterdam, The Netherlands;9. Swammerdam Institute for Life Sciences, University of Amsterdam, Amsterdam, The Netherlands |
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| Abstract: | Human-human B cell hybridoma JK32.1, constructed from B lymphocytes of a common variable immunodeficient patient and nonsecreting cell line, retains the defects of B cell immunodeficiency. Efforts to clarify whether the defect is located within the plasma membranes of this cell line were carried out by implanting them with plasma membrane fraction derived from normal functional cells via intact noninfectious Sendai virus. The implanted cells were activated with various mitogens and their Ig responses and isotype switching were examined. Restoration of IgM secretion was achieved in the implanted JK32.1 cells following stimulation with SAC, PWM, or retinoic acid. Augmented IgM response was also obtained in the implanted cells treated with retinoic acid and lipopolysaccharide (LPS) despite their unresponsiveness to LPS alone. No IgG or IgA response could be detected in the implanted JK32.1 cells. These data suggest that this immunodeficient cell line possesses at least two different malfunctions, one located within the plasma membrane moiety of the cells and the other located within the cytoplasmic and/or nucleic components. The plasma membrane moiety defect can be repaired temporarily by delivering proper signals via the implanted plasma membranes. However, this manipulation of the cells could not overcome the intrinsic defect of the cells which blocks isotype switching and secretion of IgG, IgE, and IgA antibodies. |
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