       Document 0398
 DOCN  M9610398
 TI    Both a precursor and a mature population of dendritic cells can bind
       HIV. However, only the mature population that expresses CD80 can pass
       infection to unstimulated CD4+ T cells.
 DT    9601
 AU    Weissman D; Li Y; Orenstein JM; Fauci AS; Laboratory of
       Immunoregulation, National Institute of Allergy and; Infectious
       Diseases, Bethesda, MD 20892, USA.
 SO    J Immunol. 1995 Oct 15;155(8):4111-7. Unique Identifier : AIDSLINE
       MED/96003457
 AB    Dendritic cells (DC) are the principle APC involved in primary immune
       responses; their major function is to obtain Ag in tissues, migrate to
       lymphoid organs, and activate T cells. DC are also the first immune
       cells to arrive at sites of inflammation on mucous membranes, the major
       site of sexual transmission of HIV. We have demonstrated previously that
       three populations of cells that can develop a dendritic morphology are
       present in peripheral blood. Two of these populations can express CD83,
       a marker of DC, and appear to be at different stages of maturation: 1) a
       precursor population and 2) a mature immunostimulatory DC.
       Precursor-derived DC express high levels of CD86 (B7-2) and HLA-DR but
       no CD80 (B7-1), whereas mature DC have high levels of expression of all
       three markers. Mature DC in peripheral blood bind HIV to their surface
       and induce infection when added to autologous CD4+ T cells in the
       absence of added stimuli, such as mitogens. These mature DC, when
       isolated directly from peripheral blood, appear to be conjugated to T
       cells, and these conjugates are infected easily and productively with
       HIV. These findings suggest a role for DC in early HIV infection in
       which they bind virus and interact with T cells locally or after
       migrating to a lymphoid organ, thus establishing a productive infection.
       Furthermore, they likely play a role in the propagation of HIV infection
       by activating T cells in the presence of HIV, which leads to viral
       replication and immune cell destruction.
 DE    Antigens, CD/IMMUNOLOGY  Antigens, CD80/*ANALYSIS  Cell Adhesion  Cell
       Differentiation/IMMUNOLOGY  CD4-Positive T-Lymphocytes/*VIROLOGY
       Dendritic Cells/IMMUNOLOGY/ULTRASTRUCTURE/*VIROLOGY  Human
       HIV/*METABOLISM/ULTRASTRUCTURE  HIV
       Infections/IMMUNOLOGY/TRANSMISSION/VIROLOGY  Immunoglobulins/IMMUNOLOGY
       Membrane Glycoproteins/IMMUNOLOGY  Stem Cells/IMMUNOLOGY/VIROLOGY
       JOURNAL ARTICLE

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

