Document 0159
 DOCN  M94A0159
 TI    HIV-mediated defects in immune regulation.
 DT    9412
 AU    Milman G; D'Souza MP; Division of AIDS, National Institute of Allergy
       and Infectious; Diseases, National Institutes of Health, Bethesda,
       Maryland; 20892.
 SO    AIDS Res Hum Retroviruses. 1994 Apr;10(4):421-30. Unique Identifier :
       AIDSLINE MED/94347467
 AB    The Division of AIDS (DAIDS), National Institute of Allergy and
       Infectious Diseases (NIAID), sponsored a Workshop on HIV-Mediated
       Defects in Immune Regulation on September 29-30, 1993. Workshop
       participants included investigators in basic research of immune
       regulation, animal models of HIV disease, HIV epidemiology, and HIV
       clinical research and treatment. The purpose of the workshop was to
       describe and evaluate biological mechanisms of HIV-mediated immune
       deficiency other than direct killing of infected CD4+ cells. The
       workshop focused on HIV-mediated dysfunction in signal transduction and
       in T cell development and maturation. Mechanisms by which HIV has been
       proposed to influence signal transduction include gp120 ligation to CD4,
       HIV superantigen(s), and HIV-mediated perturbations in signal pathway
       components (e.g., receptors, kinases, phosphatases, cytokines, and
       cyclins). As a result of signal dysfunction, cells may fail to respond
       to foreign antigens (anergy) or become predisposed to enter suicide
       pathways, otherwise known as programmed cell death or apoptosis.
       Programmed cell death is a normal immune regulatory mechanism that is
       activated to prevent anti-self responses and also to delete expanded but
       no longer needed cell populations. In the immune system, new cells are
       constantly produced from stem cells to replace those that die from age,
       pathological response, or programmed cell death. Dysfunction in these
       new cells may occur if HIV causes changes in the structural environment
       of the thymus and lymph nodes, or in cytokine signals.
 DE    Animal  Disease Models, Animal  Human  HIV Infections/*IMMUNOLOGY
       HIV-1/IMMUNOLOGY  Immune Tolerance  Retroviridae Infections/IMMUNOLOGY
       Signal Transduction  T-Lymphocytes/IMMUNOLOGY  MEETING REPORT  JOURNAL
       ARTICLE

       SOURCE: National Library of Medicine.  NOTICE: This material may be
       protected by Copyright Law (Title 17, U.S.Code).