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CD4 + Lymphocyte Increases in HIV Patients during Potent Antiretroviral Therapy Are Dependent on Inhibition of CD8 + Cell Apoptosis
Author(s) -
GRELLI SANDRO,
D'ETTORE GABRIELLA,
LAURIA FILIPPO,
MONTELLA FRANCESCO,
TRAGLIA LOIDE,
D'AGOSTINI CARTESIO,
LICHTNER MIRIAM,
VULLO VINCENZO,
FAVALLI CARTESIO,
VELLA STEFANO,
MACCHI BEATRICE,
MASTINO ANTONIO
Publication year - 2003
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1196/annals.1299.104
Subject(s) - apoptosis , antiretroviral therapy , cd8 , immunology , immune system , lymphocyte , lentivirus , cd4 cd8 ratio , peripheral blood mononuclear cell , cytotoxic t cell , medicine , t cell , t lymphocyte , human immunodeficiency virus (hiv) , biology , cancer research , viral load , lymphocyte subsets , viral disease , in vitro , genetics
A bstract : Although suppression of apoptosis contributes to immune‐reconstitution during potent antiretroviral therapy, its relationship with the majors indicators of response to therapy, that is, changes in CD4 + cell counts and in viral loads (VL), is still debated. We extended our previous study by collecting data on the relationships among apoptosis and immunological and virological parameters during a long‐term follow‐up of HIV patients with an overall positive response to potent antiretroviral therapy. We report results from 15 patients who completed two years of therapy. In a smaller group of patients, we focused our attention on investigating the specific contribution of the CD8 + subset in the overall changes in lymphocyte apoptosis, which occur concomitantly with the response to the therapy. Our data, while again confirming that inhibition of PBMC apoptosis is a phenomenon strictly related to a positive response to potent antiretroviral therapy, suggest that CD4 + cell rescue is not directly dependent on inhibition of CD4 + cell apoptosis but rather on that of the CD8 + subset.