Document 0501
 DOCN  M9460501
 TI    Abnormal B cell helper activity by virus-infected human CD4+ T cells.
 DT    9404
 AU    Maggi E; Almerigogna F; Del Prete G; Romagnani S; Immunologia Clinica e
       Allergologia, Istituto di Clinica Medica 3,; Universita di Firenze,
       Pisa, Italy.
 SO    Semin Immunol. 1993 Dec;5(6):449-55. Unique Identifier : AIDSLINE
       MED/94169316
 AB    Human CD4+ T cell clones infected in vitro with the human
       immunodeficiency virus (HIV), unlike their noninfected counterparts,
       induced both proliferation and immunoglobulin (Ig) production by both
       autologous and allogeneic B cells through an antigen (Ag)-nonspecific,
       MHC-unrestricted, contact-dependent mechanism. This was done apparently
       without expressing the CD40 ligand. Interestingly, HIV-infected T cell
       clones, unlike their noninfected counterparts, constitutively expressed
       mRNA for, and released in the supernatants measurable amounts of,
       TNF-alpha and a proportion of T blasts from the HIV-infected
       unstimulated T cell clones showed membrane TNF-alpha expression.
       Furthermore, both B cell proliferation and Ig production induced by
       HIV-infected unstimulated T cell clones, but not those evoked by their
       noninfected anti-CD3-stimulated counterparts, were strongly and
       consistently inhibited by either anti-TNF-alpha or anti-TNF-alpha
       receptor antibodies. Finally, when T blasts from HIV-infected
       unstimulated T cell clones were fractionated by cell sorting into
       membrane TNF-alpha-negative and membrane TNF-alpha-positive cells, only
       the latter retained the capacity to polyclonally activate B cells. Human
       CD4+ T cell clones infected in vitro with herpesvirus saimiri (HVS) also
       showed constitutive membrane TNF-alpha expression, as well as the
       ability to induce Ag-nonspecific, MHC-unrestricted, contact-dependent,
       polyclonal B cell activation. These data suggest that human CD4+ T cell
       clones, when infected by certain viruses, can provide abnormal B cell
       help that appears to be related to the expression of membrane TNF-alpha
       by virus-infected T cells.
 DE    B-Lymphocytes/*PHYSIOLOGY  Cell Communication/IMMUNOLOGY  Cells,
       Cultured  Herpesvirus 2, Saimirine/PHYSIOLOGY  Human  HIV
       Infections/*IMMUNOLOGY  Support, Non-U.S. Gov't  T-Lymphocytes,
       Helper-Inducer/*PHYSIOLOGY  Tumor Necrosis Factor/*PHYSIOLOGY  JOURNAL
       ARTICLE

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       protected by Copyright Law (Title 17, U.S.Code).