title: Role of bcl-2 and apoptosis in viral infections.
abstract: For decades immunobiologists have focussed on lymphocyte activation leading to cellular proliferation as a means by which the numbers of antigen-responsive cells can be increased. The pendulum has now swung back and questions are being raised about the way in which the size of the activated lymphocyte populations, such as those found during certain acute viral infections, can be controlled. The process of apoptosis has gained widespread recognition as a physiological means by which unwanted cells can be removed. In this review we will discuss recent observations on the control of apoptosis in the activated and expanded T cell populations found during viral infections and how this process co-exists with certain mechanisms which enable the retention of the fittest cells which can participate in subsequent encounters with virus.
authors.affiliation: Department of Clinical Immunology, Royal Free Hospital School of Medicine, London, UK.
authors.forename: A N
authors.initials: AN
authors.lastname: Akbar
authors.forename: M
authors.initials: M
authors.lastname: Salmon
authors.forename: G
authors.initials: G
authors.lastname: Janossy
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000276:immunology*; D018414:CD8-Positive T-Lymphocytes / Q000502:physiology*; D006801:Humans; D007156:Immunologic Memory; D011518:Proto-Oncogene Proteins / Q000235:genetics / Q000502:physiology*; D019253:Proto-Oncogene Proteins c-bcl-2; D014777:Virus Diseases / Q000276:immunology*
chemical_list: D011518:Proto-Oncogene Proteins; D019253:Proto-Oncogene Proteins c-bcl-2