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tially produce IL-2 (in the absence of IL-4 and IL-10), whereas CD4 CD7 ÿ T
lymphocytes produce low amounts of IL-2 and high levels of the type-2 cyto-
kines IL-4 and IL-10; additionally, lack of CD7 expression correlates with the
acquisition of CD57 on CD4 T lymphocytes (Autran et al., 1995; Legac et
al., 1992). The percentage of CD4 CD7 ÿ CD57 T lymphocytes proportionally
increases in the progression of HIV infection to AIDS (Autran et al., 1995;
Legac et al., 1992). The percentage of CD4 CD7 ÿ CD57 lymphocytes was
also shown to be signi®cantly increased when HIV-infected patients with pro-
gressive infection were compared with long-term nonprogressing individuals
(Clerici et al., 1996b).
CD30
CD30 is a member of the tumor necrosis factor ( TNF ) receptor superfamily,
which can transduce signals for proliferation, death, or nuclear factor KB (NF-
KB) activation, and whose ligand (CD30L) has been identi®ed on B cells, acti-
vated macrophages, and a subset of activated T cells. Expression of CD30 is
augmented in a number of pathologic conditions including anaplastic large cell
lymphomas, seminoma, and primary cutaneous lymphoproliferative disorders
(Ansieau et al., 1996; Romagnani, 1996). Plasma levels of CD30 are signi®-
cantly higher in HIV-1-infected patients than in controls, and are positively
correlated with those of TNF-a and soluble TNF receptors as well as with HIV
plasma viremia (Rizzardi et al., 1996). Additionally, in vitro HIV infection of
CD4 T-cell clones generated from HIV-seronegative individuals can enhance
the expression of CD30. TH2 cells preferentially express membrane CD30 and
release the soluble form of CD30; additionally, CD30-mediated signaling was
shown to promote the in vitro development of TH2-like cells (Romagnani,
1996).
Chemokine Receptors
Chemokines and their receptors are essential elements in determining the
selective attraction of various cellular subsets of leukocytes. Two such receptors
(CCR5 and CXCR4) have gained a pivotal role in the pathogenesis of HIV
infection as they have been identi®ed as the main coreceptors allowing the
intracellular penetration of (respectively) monocytotropic and lymphotropic
strains of HIV into target cells ( Berger et al., 1999; Garzino-Demo et al., 1998;
Loetscher et al., 2000). Polarized TH1 and TH2 cells were recently shown to
di¨erentially express chemokine receptors. Thus, the expression of CCR4 and
CCR8 on TH2 cells was observed to be transiently increased following TCR
and CD28 engagement; additionally, the response of TH2 cells to I-309 (CCR8
ligand) and thymus- and activation-regulated chemokine ( TARC) (CCR4 and
CCR8 ligand) was shown to be enhanced (Dambrosio et al., 1998). Other
results showed that 1) naive T cells express CXCR4, whereas the majority of
memory/activated T cells express CXCR3; 2) TH1-polarized T-cell lines ex-
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