       Document 0598
 DOCN  M9640598
 TI    Differential patterns of T-cell receptor BV-specific activation of T
       cells by gp120 from different HIV strains.
 DT    9604
 AU    Akolkar PN; Gulwani-Akolkar B; Silver J; Department of Medicine, North
       Shore University Hospital/Cornell; University Medical College,
       Manhasset, New York, USA.
 SO    Scand J Immunol. 1995 Dec;42(6):598-606. Unique Identifier : AIDSLINE
       MED/96150309
 AB    Studies by several groups have suggested that HIV infection in vivo
       results in a BV-specific alteration of the TCR repertoire and that this
       might play a role in the pathogenesis of AIDS. Our earlier studies
       demonstrated that both a crude extract of HIV451 as well as purified gp
       160 from HIV451 could specifically activate, in vitro, T cells
       expressing a common set of TCRBV segments (TCRBV3, 12, 14, 15, and
       sometimes BV17 and 20) in individuals of disparate HLA type.
       Furthermore, purified gp120 from HIV451 was shown to have a similar
       ability to activate T cells, although with a slightly different
       TCRBV-specific pattern. In order to determine whether gp120 from other
       HIV strains could similarly activate T cells in a TCRBV-specific
       pattern, PBMC from HIV seronegative individuals of disparate HLA type
       were stimulated with gp120 from three strains of HIV (451, IIIB, and
       MN). The authors found that gp120 from all three strains activate T
       cells bearing TCRBV2 and BV3 in nearly every individual. T cells
       expressing other BV segments are also activated, but this is more
       variable and appears to be unique to each individual. Furthermore,
       gp120(451) and gp120 from HIVIIIB and HIVMN differ in their ability to
       activate T cells expressing these other TCRBV segments. These
       observations suggest that variation in the structure of gp120 and in the
       genetic and/or environmental background of the individual play an
       important role in determining which TCRBV segments are 'triggered' by
       gp120. Furthermore, these observations may have important implications
       for the rate of disease progression in HIV-infected individuals.
 DE    Cells, Cultured  Human  HIV/*IMMUNOLOGY  HIV Envelope Protein
       gp120/*IMMUNOLOGY  Leukocytes, Mononuclear/IMMUNOLOGY  *Lymphocyte
       Transformation  Receptors, Antigen, T-Cell, alpha-beta/*IMMUNOLOGY
       Recombinant Proteins/IMMUNOLOGY  Reproducibility of Results  Species
       Specificity  Support, U.S. Gov't, P.H.S.  T-Lymphocytes/*IMMUNOLOGY
       JOURNAL ARTICLE

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

