       Document 0945
 DOCN  M9540945
 TI    Macrophage-colony stimulating factor (M-CSF) stimulation induces cell
       death in HIV-infected human monocytes.
 DT    9504
 AU    Bergamini A; Capozzi M; Piacentini M; Department of Public Health and
       Cell Biology, University of Rome; Tor Vergata, Italy.
 SO    Immunol Lett. 1994 Sep;42(1-2):35-40. Unique Identifier : AIDSLINE
       MED/95130139
 AB    We show here that HIV-infected monocyte-macrophages stimulated by
       macrophage-colony stimulating factor (M-CSF) undergo massive syncytia
       formation and die. The M-CSF-stimulated HIV-infected
       monocyte-macrophages (M/M) destroy themselves by blebbing out particles
       (resembling apoptotic bodies) which may contain condensed and marginated
       chromatin. The death of monocyte-macrophages is also characterized by
       the expression of Tissue Transglutaminase (tTG) which is one of the
       genes specifically expressed and activated in apoptising cells.
       Noteworthy, when the syncytia formation and consequently death is
       prevented, infected monocyte-macrophages remain viable and produce large
       amounts of virus for an extended period. The concentrations of M-CSF
       (1000 U/ml) used in this work are similar to those that stimulate
       macrophages in vivo. This suggests that HIV killing of M/M in the
       presence of M-CSF could lead, in vivo, to a greater than expected loss
       of immune cells and may contribute to explain the complex derangement of
       the immune function observed in HIV-infected patients.
 DE    Cell Death/*IMMUNOLOGY  Cell Survival  Cells, Cultured  Cytopathogenic
       Effect, Viral  Human  HIV Core Protein p24/METABOLISM  HIV-1/*IMMUNOLOGY
       Immunoenzyme Techniques  Macrophage Colony-Stimulating
       Factor/*IMMUNOLOGY  Macrophages/ENZYMOLOGY/IMMUNOLOGY/*VIROLOGY
       Monocytes/ENZYMOLOGY/IMMUNOLOGY/*VIROLOGY  Protein-Glutamine
       gamma-Glutamyltransferase/METABOLISM  Support, Non-U.S. Gov't  JOURNAL
       ARTICLE

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

