       Document 0529
 DOCN  M9620529
 TI    Triggering of complement receptors CR1 (CD35) and CR3 (CD11b/CD18)
       induces nuclear translocation of NF-kappa B (p50/p65) in human monocytes
       and enhances viral replication in HIV-infected monocytic cells.
 DT    9602
 AU    Thieblemont N; Haeffner-Cavaillon N; Haeffner A; Cholley B; Weiss L;
       Kazatchkine MD; INSERM U430, Broussais Hospital, Paris, France.
 SO    J Immunol. 1995 Nov 15;155(10):4861-7. Unique Identifier : AIDSLINE
       MED/96062305
 AB    Monocyte/macrophages may harbor HIV in a nonproductive fashion for
       prolonged periods of time. Viral gene expression may be reactivated by
       stimulation of the cells with LPS or cytokines such as TNF-alpha in
       vitro. The effect of LPS and TNF-alpha is mediated by their ability to
       induce nuclear translocation of the DNA-binding heterodimer NF-kappa B
       (p50/p65), which binds to a specific sequence in the HIV-long terminal
       repeat. The present study demonstrates that triggering of complement
       receptors CR1 (CD35) and CR3 (CD11b/CD18) enhances viral replication in
       HIV-infected human monocytic cells. Monocytic cell lines and normal
       peripheral blood monocytes were infected with HIV-1 in vitro and
       cultured in the presence or absence of F(ab')2 fragments of monoclonal
       anti-CR1 or anti-CR3 Abs or with C3 fragments. Stimulation of CR1 or CR3
       induces a two- to fourfold increase in the amount of cell-associated and
       released p24 Ag in cell cultures that was equivalent to that observed in
       control cultures triggered with LPS. We further observed that
       stimulation of CR1 or CR3 induces the nuclear translocation of NF-kappa
       B p50/p65 in infected cells. Translocation of NF-kappa B p50/p65 was
       also observed following stimulation of CR1 or CR3 of uninfected
       peripheral blood monocytes from HIV-seronegative donors. The amount of
       protein translocated was similar to that observed when cells were
       stimulated with rhTNF-alpha. TNF-alpha did not mediate the translocation
       of NF-kappa B p50/p65 induced by triggering of complement receptors.
       Taken together, these observations suggest that HIV gene expression may
       be activated in infected monocytes through interaction of the cells with
       complement-opsonized particles and that enhanced viral replication is
       associated with C3 receptor-mediated nuclear translocation of the
       NF-kappa B complex.
 DE    Antigens, CD11/*PHYSIOLOGY  Biological Transport  Cell
       Nucleus/PHYSIOLOGY  Cells, Cultured  *DNA Replication  Human  HIV
       Infections/IMMUNOLOGY/*PHYSIOPATHOLOGY  HIV-1/*PHYSIOLOGY
       Monocytes/PHYSIOLOGY/*VIROLOGY  NF-kappa B/*PHYSIOLOGY  Receptors,
       Complement 3b/*PHYSIOLOGY  Support, Non-U.S. Gov't  *Virus Replication
       JOURNAL ARTICLE

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

