Document 0116
 DOCN  M9460116
 TI    Envelope glycoproteins of HIV-1 interfere with T-cell-dependent B cell
       differentiation: role of CD4-MHC class II interaction in the effector
       phase of T cell help.
 DT    9408
 AU    Chirmule N; Wang XP; Hu R; Oyaizu N; Roifman C; Pahwa R; Kalyanaraman
       VS; Pahwa S; Department of Pediatrics, North Shore University Hospital,;
       Cornell University Medical College, Manhasset, New York 11030.
 SO    Cell Immunol. 1994 Apr 15;155(1):169-82. Unique Identifier : AIDSLINE
       MED/94221655
 AB    T-cell-dependent B cell differentiation involves two phases: an
       inductive phase of T cell activation followed by an effector phase,
       which involves stimulation of B cells by activated T cells. We have
       previously demonstrated that anti-CD3 mAb and antigen-induced
       T-cell-dependent B cell functions are inhibited by HIV-1 envelope
       glycoprotein, gp120, at the inductive phase of T-cell-dependent B cell
       response. In this study we have investigated whether gp120 also inhibits
       the effector phase of interactions involved in T-cell-dependent-B cell
       differentiation response. For these studies, CD4+ T cells were first
       activated with antigen or pokeweed mitogen, cultured with soluble
       HIV-gp120 or medium for 2 hr, and washed. Coculture of gp120-treated
       preactivated T cells with autologous B cells resulted in impairment of
       IgG secretion, but did not affect IgM secretion significantly. The IgG
       secretion was restored by the addition of PMA (activator of protein
       kinase C) or forskolin (activator of adenylate cyclase), but not by the
       addition of ionomycin (inducer of intracellular calcium) to the T plus B
       cell cultures. A similar pattern of Ig secretion (IgM, no IgG) was
       observed with B cells of a patient with bare lymphocyte syndrome,
       indicating a requirement for MHC class II molecule interaction with T
       cells. These studies suggest that the effector phase of T-B cell
       interactions are impaired by gp120, and that the mechanism involves a
       signal transducing event(s), which is dependent upon cyclic AMP and/or
       protein kinase C. Furthermore, these latter reactions occur subsequent
       to T-B cell contact-dependent interactions at the effector phase, which
       involve MHC class II molecules on B cells and CD4 molecules on T cells.
 DE    Antigen Presentation  Antigens, CD4/IMMUNOLOGY
       B-Lymphocytes/*IMMUNOLOGY  Cell Communication  Cell
       Differentiation/*DRUG EFFECTS  Cytokines/PHARMACOLOGY  Female
       Histocompatibility Antigens Class II/IMMUNOLOGY  Human  HIV Envelope
       Protein gp120/*PHARMACOLOGY  IgG/BIOSYNTHESIS  IgM/BIOSYNTHESIS  Infant
       Lymphocytes/PATHOLOGY  Signal Transduction  Support, U.S. Gov't, P.H.S.
       T-Lymphocytes/*DRUG EFFECTS/*IMMUNOLOGY  T-Lymphocytes,
       Helper-Inducer/DRUG EFFECTS/IMMUNOLOGY  JOURNAL ARTICLE

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