Awardee OrganizationWEILL MEDICAL COLL OF CORNELL UNIV
Description
Abstract Text
DESCRIPTION:
Superantigens (SA) are microbial glycoproteins that act as potent T cell
activators. They bind to major histocompatibility complex (MHC) class
II proteins, but T cell recognition of SA is not restricted by MHC
alleles, and there is no requirement for antigen processing, as with
regular peptide antigens. Typically, alpha-beta T cell antigen receptors
(TCR) of T cells responding to a given SA express the same V beta
variable region gene products. Thus SA are also called V beta-selective
elements.
By preparing a panel of monoclonal antibodies to human V beta gene
products, the investigators have developed a novel technique for rapid
isolation of homogeneous cell lines expressing the same V beta. These
IL-2 dependent non- transformed cells were used as targets for HIV-1
infection in vitro. HIV replication measured by gag encoded p24 varied
up to 100 fold depending on V beta expression with V beta 12, but not V
beta 6.7a cell lines, supporting high level HIV-1 replication of three
divergent isolates. This effect is not MHC restricted and can be blocked
with anti-MHC class II mAb. Using ex vivo lymphocytes from seropositive
donors they found that V beta 12 cells expressed more gp120 and contained
more HIV-l DNA than control V beta subsets. Non-T cells from such donors
selectively stimulated a V beta 12 cell line and not a V beta 6.7a cell
line consistent with expression of a SA.
They propose to (l) define the HIV-1 associated SA using divergent and
defective viral isolates. In particular, they will use two isolates with
different V beta specificity patterns to produce chimeras and map the
gene encoding V beta selectivity; and (2) investigate the functional
effects of the HIV-l SA. They propose experiments to compare the HIV-V
beta selective element to microbial SA, to examine the effects of the
possible SA in vivo in HIV-1 seropositive patients, in HIV-l infected
hu/SCID mice, and in TCR V beta 12 and TCR V beta 6.7a transgenic mice.
They suggest that blocking the effects of an HIV-1 SA in vivo could
represent a novel therapeutic approach to AIDS.
National Institute of Allergy and Infectious Diseases
CFDA Code
DUNS Number
060217502
UEI
YNT8TCJH8FQ8
Project Start Date
01-April-1993
Project End Date
31-March-1996
Budget Start Date
01-April-1994
Budget End Date
31-March-1995
Project Funding Information for 1994
Total Funding
$283,113
Direct Costs
$167,579
Indirect Costs
$115,534
Year
Funding IC
FY Total Cost by IC
1994
National Institute of Allergy and Infectious Diseases
$283,113
Year
Funding IC
FY Total Cost by IC
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