Fas and FasL in the homeostatic regulation of immune responses |
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| Affiliation: | 1. Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, CA;2. Centre for Medical Parasitology, Department of International Health, Immunology & Microbiology, University of Copenhagen and Department of Infectious Diseases, Rigshospitalet, Copenhagen, Denmark;1. Center for Cell and Gene Therapy, Baylor College of Medicine, Houston Methodist Hospital and Texas Children’s Hospital, Houston, TX, USA;1. Resident, Department of Plastic and Reconstructive Surgery, Hotel Dieu de France Hospital, Beirut, Lebanon;2. Resident, Department of Plastic and Reconstructive Surgery, Hotel Dieu de France Hospital, Beirut, Lebanon;3. Assistant Professor, Department of Plastic and Reconstructive Surgery, Hotel Dieu de France Hospital, Beirut, Lebanon;4. Department Head, Department of Plastic and Reconstructive Surgery, Hotel Dieu de France Hospital, Beirut, Lebanon;1. Medical University of South Carolina, Charleston, SC, United States;2. The University of Texas MD Anderson Cancer Center, Houston, TX, United States;1. Division of Immunology, The Netherlands Cancer Institute, Amsterdam, The Netherlands;2. Center for Chronic Immunodeficiency (CCI), University Medical Center Freiburg and University of Freiburg, Freiburg, Germany;3. From the Arkansas Biosciences Institute, Department of Biological Sciences, Arkansas State University, Jonesboro, Arkansas 72467,;4. the Department of Neurology, Thomas Jefferson University, Philadelphia, Pennsylvania 19107,;5. the Department of Veterinary Pathobiology, University of Missouri, Columbia, Missouri 65211,;6. the Laboratory of Genetics, NIA-Intramural Research Program, National Institutes of Health, Baltimore, Maryland 21224,;12. the Department of Neurobiology and Developmental Sciences, College of Medicine, University of Arkansas for Medical Sciences, Little Rock, Arkansas 72205, and;8. the Arkansas Biosciences Institute, Arkansas State University, Jonesboro, Arkansas 72467 |
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| Abstract: | ![]()
Studies of the biological effects of Fas signaling, using transformed cell lines as targets, indicate that ligation of the Fas receptor induces an apoptotic death signal. Chronically activated normal human T cells are also susceptible to Fas-mediated apoptosis. However, interactions between Fas and Fas ligand can also yield a costimulatory signal. Here, David Lynch, Fred Ramsdell and Mark Alderson present a model for the role of Fas and FasL in the homeostatic regulation of normal immune responses. They discuss how dysregulation of the Fas apoptotic pathway may contribute to certain disease states, including autoimmune disease and human immunodeficiency virus (HIV)-induced depletion of CD4+ T cells. |
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