Important note: Information in this article was accurate in 1988. The state of the art may have changed since the publication date.
IMMUNOPATHOGENESIS OF THE ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)
Progress in Immunology VI. Sixth International Congress of Immunology. Cinader B, Miller RG, eds. New York, Academic Press, p. 949-60, 1986.. Unique Identifier : AIDSLINE ICDB/88640053 Margolick JB; Fauci AS; Dept. of Environmental Health Sciences, The Johns Hopkins Sch. of; Hygiene and Public Health, Baltimore, MD 21205
Abstract:
The immunopathogenesis of acquired immunodeficiency syndrome (AIDS) is reviewed under the following headings: quantitative T lymphocyte deficiency, qualitative abnormalities of T lymphocytes, inhibition of CD4+ cell function, activated T cells and cofactors in the pathogenesis of AIDS, abnormalities in B lymphocytes and monocytes, and serologic abnormalities and circulating suppressor factors. AIDS is characterized by a host of abnormalities in the function of CD4 surface antigen-positive lymphocytes. A selective defect in the subset of T4+ cells responsible for antigen recognition is compounded by abnormalities in antigen-presenting cells (monocyte/macrophages) resulting from insufficient production of lymphokines, and possibly direct infection with human T lymphotropic virus (HTLV)-III/lymphadenopathy-associated virus (LAV). B cells also are abnormal in that they are polyclonally activated, possibly due to a direct effect of HTLV-III/LAV or viral components, and are defective in their response to de novo antigens. Abnormalities of natural killer cells and cytotoxic T cells probably reflect a defect in inductive signals normally delivered by the CD4+ cell. Some of the monocyte and cytotoxic cell functional abnormalities can be corrected in vitro by CD4- cell-derived soluble mediators such as interleukin-2 and interferon-gamma, further implicating the lack of an inductive CD4+ cell signal as the cause of these abnormalities. Following infection of certain CD4+ cell lines with HTLV-III/LAV, a small proportion of the infected cells survive and harbor latent viral genetic material. These cells can be induced to produce infectious virus under appropriate conditions, a finding which has important implications for the understanding of the natural history of HTLV-III/LAV and for developing therapies for HTLV-III/LAV infection. (77 Refs)
Keywords: Acquired Immunodeficiency Syndrome/*IMMUNOLOGY B-Lymphocytes/IMMUNOLOGY Cell Line Human HIV/*IMMUNOLOGY Leukocyte Count Lymphocyte Transformation Monocytes/IMMUNOLOGY T-Lymphocytes/*IMMUNOLOGY T-Lymphocytes, Helper-Inducer/IMMUNOLOGY T-Lymphocytes, Suppressor-Effector/IMMUNOLOGY MEETING PAPER
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Important note: Information in this article was accurate in 1988. The state of the art may have changed since the publication date.
