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were also reported in HIV
persons. Hinz et al. reported that whereas 80% of
all gd T cell from HIV
ÿ
persons express Vg9 chain, only 10% of the gd T cells
in HIV
persons reacted with the anti-Vg9 monoclonal antibody (mAb). Most
gd T cells in HIV-1 infected individuals were Vg9/Vg2/Vg3orVg4 negative and
thus they expressed either Vg5orVg8, which are rarely found among periph-
eral blood lymphocytes in healthy adults ( Hinz et al., 1994). More recently,
analysis of Vg gene usage by both ¯ow cytometry and polymerase chain reac-
tion ( PCR) revealed that all VgI genes (i.e., Vg2, 3, 4, 5, and 8) were expressed
in higher percentages in HIV
when compared with HIV
ÿ
persons. In contrast,
VgII gene ( Vg9) expression was markedly reduced. In addition, no preferential
association between Vd1 with a particular Vg gene was observed (Wesch et al.,
1998).
Characterization of Vd1-J1 junctional diversity in peripheral lymphocytes of
HIV-infected persons demonstrated the stability of the Vd1 repertoire over
time and suggested the absence of a CDR3-dependent antigenic selection of this
subset (Boullier et al., 1995).
The analysis of Vd1 CDR3 size distribution and comparison of Vd1-Jd
junctional sequences showed both restricted and unrestricted patterns in HIV
and HIV
ÿ
persons. Thus, the Vd1 predominance in HIV
persons does not
seem to be a consequence of an HIV-1 speci®c clonal expansion ( Boullier et al.,
1997; Hinz et al., 1994).
Phenotypic analysis of gd T cells from peripheral blood and bone marrow at
di¨erent stages of the HIV infection showed that a large fraction of Vd1 T cells
from HIV
individuals display the phenotype of activated cells. Vd1 T cells
from HIV
persons frequently coexpress CD8 and CD38 and CD45RO and
HLA-DR, although expression of the IL-2 receptor (CD25) was not higher
than that found on Vd1 T cells from HIV
ÿ
controls (Boullier et al., 1995;
Rossol et al., 1998). HLA-DR, CD8, and CD45RO expression did not vary
with the stages of HIV spectrum. In addition to activation markers, Vd1 T cells
from HIV-infected individuals showed an increased capacity to expand in re-
sponse to IL-2 ( Boullier et al., 1995).
Origin of the Expanded Circulating V
d
1 T Cells in HIV Infection
The origin of the expanded blood Vd1 T-cell pool in HIV infection is unknown.
Comparative analysis of phenotype and TCR repertoire in lymph node ( LN )
and blood showed that these Vd1 populations di¨er in activation marker ex-
pression and in Vd1 repertoire ( Boullier et al., 1997). Both populations ex-
pressed CD38, however LN gd T cells did not express CD45RO (memory
marker). Furthermore, there were di¨erences in the Vd1-Jd1 CDR3 size distri-
bution between the two gd T-cell populations, with the LN Vd1 T cells showing
a Gaussian CDR3 size distribution. This suggests that the lymph node is not a
site of Vd1 T-cell activation in HIV-infected persons.
One interesting hypothesis postulates that blood Vd1 T cells originate in the
