Open AccessComparison of activation marker and TCR Vβ gene product expression by CD4 + and CD8 + T cells in peripheral blood and lymph nodes from HIV‐infected patients
Author(s) -
RAMZAOUI S.,
JOUENBEADES F.,
MICHOT F.,
BORSALEBAS F.,
HUMBERT G.,
TRON F.
Publication year - 1995
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.1995.tb05530.x
Subject(s) - cd8 , cd38 , t cell receptor , immunology , biology , t cell , lymph , antigen , t lymphocyte , flow cytometry , cytotoxic t cell , microbiology and biotechnology , immune system , pathology , medicine , genetics , in vitro , stem cell , cd34
SUMMARY Since lymphoid organs constitute the site of active and progressive HIV disease, analysis of their lymphocytes may provide more accurate information on T cell abnormalities than that obtained from studying peripheral blood lymphocytes. The objective of this study was to compare the expressions of activation markers and T cell receptor (TCR) Vβ gene products by CD4 + and CD8 + T cells in lymph nodes (LN) and peripheral blood (PB) from healthy individuals and asymptomatic HIV‐infected patients to determine whether anomalies that could be identified at the HIV replication site could support the hypothesis of T cell activation by HIV‐encoded antigens or superantigens. CD4 + and CD8 + T cells in paired LN and PB obtained from six healthy controls and five asymptomatic HIV‐infected individuals were analysed by flow cytometry, using anti‐CD38, anti‐HLA‐DR and 13 anti‐Vβ MoAbs that cover, approximately, 45% of the T cell repertoire. Analysis of T cell activation marker expression indicated that the percentages of CD4 + and CD8 + T cells bearing CD38 or CD38 and HLA‐DR molecules were higher in patients than in controls and, in patients, higher in LN than in PB. Comparison between the Vβ repertoires of CD4 + and CD8 + T cells in LN and PB showed that, in each healthy individual, a limited number of Vβ families expressed by CD4 + or CDS + T cells had different repartition in LN and PB, whereas in each HIV + patient, more Vβ families exhibited different distributions and these differences recurred among certain Vβ segments, such as Vβ5.3 and Vβ21 in the CD4 + T cell population and Vβ5.2/5.3, Vβ12 and Vβ12 in the CD8 + T cell population. Taken together, these data argue for a skewed TCR repertoire in HIV infection and sustained activation of T cells by HIV‐encoded antigens at the site of HIV replication, and further demonstrate that a high proportion of CD4 + T cells are in an activation state that may, indirectly, participate in their functional abnormalities.