TY - JOUR
T1 - Basic and clinical immunology
T2 - Markers of cell death-activation in lymphocytes of vertically HIV-infected children naive to highly active antiretroviral therapy: The role of age
AU - Viganò, Alessandra
AU - Pinti, Marcello
AU - Nasi, Milena
AU - Moretti, Laura
AU - Balli, Fiorella
AU - Mussini, Cristina
AU - Bricalli, Dorella
AU - Sala, Natascia
AU - Bugarini, Roberto
AU - Vella, Stefano
AU - Principi, Nicola
AU - Cossarizza, Andrea
PY - 2001
Y1 - 2001
N2 - Background: Apoptosis plays a major role in depleting CD4 + lymphocytes during infection with HIV-1. Few data exist on its role during HIV infection of children. Sensitivity of peripheral blood lymphocytes (PBLs) to apoptotic stimuli and the importance of the patient's age remain unclear. Objectives: We sought to analyze the following: (1) markers of cell death-activation (CD95, CD45 isoforms, and CD28) in PBLs from vertically HIV-infected children of different ages before highly active antiretroviral therapy; (2) changes in other PBL populations; (3) PBL sensitivity to cell death and mitochondrial damages; and (4) role of age during progression of infection. Methods: Cell culture techniques and flow cytometry were used to analyze surface antigens, PBL susceptibility to apoptosis, or PBL susceptibility to change of mitochondrial membrane potential. Results: Donor age had a strong negative correlation with numbers of CD4 + and CD8 + T cells. Virgin T lymphocyte (CD45RA +, CD95 -) levels and those of CD95 + cells showed no correlation with the children's clinical status but did show a correlation with patient age. CD28 - T lymphocytes were markedly augmented in HIV-infected children but were unrelated to stage of infection or age. A relevant decrease in B lymphocytes and an increase in natural killer cells were also found. Finally, PBLs from HIV-positive children had a marked tendency to undergo apoptosis and mitochondrial damage. Conclusion: Changes in PBL phenotype, increased expression of CD95, and high sensitivity to apoptosis suggest that a precocious aging of the immune system occurs in HIV-infected children.
AB - Background: Apoptosis plays a major role in depleting CD4 + lymphocytes during infection with HIV-1. Few data exist on its role during HIV infection of children. Sensitivity of peripheral blood lymphocytes (PBLs) to apoptotic stimuli and the importance of the patient's age remain unclear. Objectives: We sought to analyze the following: (1) markers of cell death-activation (CD95, CD45 isoforms, and CD28) in PBLs from vertically HIV-infected children of different ages before highly active antiretroviral therapy; (2) changes in other PBL populations; (3) PBL sensitivity to cell death and mitochondrial damages; and (4) role of age during progression of infection. Methods: Cell culture techniques and flow cytometry were used to analyze surface antigens, PBL susceptibility to apoptosis, or PBL susceptibility to change of mitochondrial membrane potential. Results: Donor age had a strong negative correlation with numbers of CD4 + and CD8 + T cells. Virgin T lymphocyte (CD45RA +, CD95 -) levels and those of CD95 + cells showed no correlation with the children's clinical status but did show a correlation with patient age. CD28 - T lymphocytes were markedly augmented in HIV-infected children but were unrelated to stage of infection or age. A relevant decrease in B lymphocytes and an increase in natural killer cells were also found. Finally, PBLs from HIV-positive children had a marked tendency to undergo apoptosis and mitochondrial damage. Conclusion: Changes in PBL phenotype, increased expression of CD95, and high sensitivity to apoptosis suggest that a precocious aging of the immune system occurs in HIV-infected children.
KW - Apoptosis
KW - CD95
KW - CD95L
KW - HIV
KW - Mitochondria
KW - Pediatric AIDS
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U2 - 10.1067/mai.2001.117791
DO - 10.1067/mai.2001.117791
M3 - Article
C2 - 11544465
AN - SCOPUS:0034834856
VL - 108
SP - 439
EP - 445
JO - Journal of Allergy and Clinical Immunology
JF - Journal of Allergy and Clinical Immunology
SN - 0091-6749
IS - 3
ER -