Objective: To analyse variation in T-cell receptor (TCR) Vbeta gene expression in T cells in HIV-infected individuals. Design: Because there are very few monoclonal antibodies available for studying TCR Vbeta gene expression, we used polymerase chain reaction (PCR) to analyse the TCR Vbeta repertoire in HIV-infected individuals using specific primers for 20 distinct families of TCR Vbeta. Methods: Evaluation of TCR Vbeta gene expression in peripheral blood from HIV-1-infected individuals [two in Centers for Disease Control (CDC) stage II, five in CDC stage III and four in CDC stage IV]. Complementary DNA was produced from CD4+ and CD8+ T cells, amplified by PCR and analysed after Southern blotting and hybridization with a Cbeta-specific oligonucleotide probe. Results: Vbeta gene expression was dramatically modified, especially in AIDS patients. The CD4+ T-cell subset showed both overexpression (Vbeta2) and deletions or underexpression (Vbeta9-Vbeta20), whereas these gene segments were expressed normally in the CD8+ subset. Only Vbeta 3 was deleted or underexpression in both CD4+ and CD8+ populations in AIDS patients. Conclusions: HIV-1 infection induces CD4+ T-cell deficiency, both in total numbers and by causing a paucity of select Vbeta gene expression in this subset. In addition, the Vbeta3 gene family was deleted or underexpressed was observed in both CD4+ and CD8+ T-cell subsets from patients in CDC stage IV. These results are compatible with changes in Vbeta gene expression known to occur under the action of endogenous or exogenous superantigens.
HIV infection leads to differential expression of T-cell receptor V-beta genes in CD4+ and CD8+ T cells
ESIN, SEMIH;
1993-01-01
Abstract
Objective: To analyse variation in T-cell receptor (TCR) Vbeta gene expression in T cells in HIV-infected individuals. Design: Because there are very few monoclonal antibodies available for studying TCR Vbeta gene expression, we used polymerase chain reaction (PCR) to analyse the TCR Vbeta repertoire in HIV-infected individuals using specific primers for 20 distinct families of TCR Vbeta. Methods: Evaluation of TCR Vbeta gene expression in peripheral blood from HIV-1-infected individuals [two in Centers for Disease Control (CDC) stage II, five in CDC stage III and four in CDC stage IV]. Complementary DNA was produced from CD4+ and CD8+ T cells, amplified by PCR and analysed after Southern blotting and hybridization with a Cbeta-specific oligonucleotide probe. Results: Vbeta gene expression was dramatically modified, especially in AIDS patients. The CD4+ T-cell subset showed both overexpression (Vbeta2) and deletions or underexpression (Vbeta9-Vbeta20), whereas these gene segments were expressed normally in the CD8+ subset. Only Vbeta 3 was deleted or underexpression in both CD4+ and CD8+ populations in AIDS patients. Conclusions: HIV-1 infection induces CD4+ T-cell deficiency, both in total numbers and by causing a paucity of select Vbeta gene expression in this subset. In addition, the Vbeta3 gene family was deleted or underexpressed was observed in both CD4+ and CD8+ T-cell subsets from patients in CDC stage IV. These results are compatible with changes in Vbeta gene expression known to occur under the action of endogenous or exogenous superantigens.I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.
