V-DELTA-1 T-CELLS EXPANDED IN THE BLOOD THROUGHOUT HIV-INFECTION DISPLAY A CYTOTOXIC ACTIVITY AND ARE PRIMED FOR TNF-ALPHA AND IFN-GAMMA PRODUCTION BUT ARE NOT SELECTED IN LYMPH-NODES

Citation
S. Boullier et al., V-DELTA-1 T-CELLS EXPANDED IN THE BLOOD THROUGHOUT HIV-INFECTION DISPLAY A CYTOTOXIC ACTIVITY AND ARE PRIMED FOR TNF-ALPHA AND IFN-GAMMA PRODUCTION BUT ARE NOT SELECTED IN LYMPH-NODES, The Journal of immunology, 159(7), 1997, pp. 3629-3637
Citations number
73
Categorie Soggetti
Immunology
Journal title
The Journal of immunology
ISSN journal
00221767 → ACNP
Volume
159
Issue
7
Year of publication
1997
Pages
3629 - 3637
Database
ISI
SICI code
0022-1767(1997)159:7<3629:VTEITB>2.0.ZU;2-X
Abstract
We have previously reported significant alterations of gamma delta sub set distribution in the peripheral blood of HIV-infected donors. These modifications are characterized by the depletion of the V delta 2 sub set associated with a strong increase in peripheral V delta 1 T cells, In addition, the latter exhibit ex vivo an activated phenotype and sh ow a restricted complementarity-determining region 3 (CDR3) repertoire , In the present report we first address the question of the origin of these expanded cells. The lack of expansion and the Gaussian compleme ntarity-determining region 3 size distribution of lymph node V delta 1 T cells suggest that lymph nodes do not represent the site of specifi c activation of this subset, The function of blood V delta 1 T cells w as also explored. We report that patients' V delta 1 T cells express h igh levels of perforin and display an in vitro cytotoxic activity, who se characteristics are different from those of NK and LAK cells. In ad dition, single cell analysis of cytokine production revealed that, in contrast to V delta 1 T cells from control donors, patients' V delta 1 T cells are primed in vivo for IFN-gamma and TNF-alpha production. To gether, these results indicate that in the course of HIV infection, ex panded blood V delta 1 T cells are differentiated into a functional su bset and raise the question of the contribution of this subset to AIDS pathogenesis.