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T cell receptor Vβ repertoire in HIV‐infected individuals: lack of evidence for selective Vβ deletion
Author(s) -
BOYER V.,
SMITH L. R.,
FERRE F.,
PEZZOLI P.,
TRAUGER R. J.,
JENSEN F. C.,
CARLO D. J.
Publication year - 1993
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.1365-2249.1993.tb03417.x
Subject(s) - superantigen , t cell receptor , biology , immunology , t cell , enterotoxin , receptor , virology , gene , immune system , genetics , escherichia coli
SUMMARY The gradual decline of CD4 + T lymphocytes in HIV‐infected individuals culminates in the lethal immunosuppression of AIDS. The mechanism of CD4 + T cell loss is currently unknown, but has recently been suggested to occur as a result of an HIV‐encoded superantigen which facilitates a selective deletion of T cells expressing specific Vβ genes. To verify and extend such observations, peripheral blood leucocytes (PBL) from 15 CD4 + individuals, 10 of which had very low CD4 T cell counts (< 200/mm 3 ), were analysed for T cell receptor (TCR) V/β gene expression. In contrast to a recent study, the results presented here fail to provide evidence that selective loss of Vβ‐bearing T cells occurs in HIV + individuals. Furthermore, when PBL from HIV + individuals were stimulated with Staphylococcal enterotoxin B (SEB), T cells expressing Vβ subfamilies known to engage this superantigen were expanded, indicating that such cells were not deleted and were responsive to stimulation by a bacterial superantigen. Collectively, these data suggest that CD4 loss in HIV patients docs not occur in a Vβ‐seleetive, superantigen‐mediated fashion.

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