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Clinical and Diagnostic Laboratory Immunology, March 1998, p. 230-234, Vol. 5, No. 2
Departments of Pediatrics,1
Medicine,2 and
Microbiology and
Immunology,5
The Jonsson Comprehensive
Cancer Center,3 and
University of
California Los Angeles AIDS Institute,4
University of California Los Angeles School of Medicine, Los
Angeles, California
Received 7 August 1997/Returned for modification 19 September
1997/Accepted 1 December 1997
Apoptosis continues to be controversial in human immunodeficiency
virus (HIV)-induced pathogenesis. To investigate whether apoptosis
occurs with HIV exposure with or without subsequent infection, levels
of apoptosis were measured in cord blood lymphocytes (CBL) from seven
newborns delivered to HIV-infected mothers and seven normal, unexposed
newborns. Live cells were costained with antibodies to cell surface
markers and the DNA dye 7-amino actinomycin D to immunophenotype
apoptotic CBL subsets. Apoptosis was measured in fresh and cultured CBL
in the presence and absence of CD3 T-cell receptor stimulation.
Compared to the CD4+ CBL from HIV-unexposed newborns,
CD4+ CBL from six HIV-exposed, noninfected newborns
demonstrated significantly greater apoptosis after overnight culture
even in the absence of CD3 stimulation. Compared to HIV-unexposed
controls, CD8+ CBL from the six HIV-exposed newborns also
demonstrated increased levels of apoptosis after overnight culture
without stimulation. The one HIV-infected newborn in this study showed
the highest levels of CD4+ and CD8+ apoptotic
CBL. The data suggest that levels of apoptosis are increased in infants
in association with HIV infection. Furthermore, CD4+ and
CD8+ cord blood lymphocytes from HIV-exposed infants
behaved differently than T lymphocytes from either normal, unexposed
infants or an HIV-infected infant. These results suggest that exposure
to HIV or HIV-induced factors increases the levels of apoptosis in CBL.
1071-412X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Apoptosis in Cord Blood T Lymphocytes from Infants
of Human Immunodeficiency Virus-Infected Mothers

*
Corresponding author. Mailing address: Department of
Microbiology and Immunology, UCLA School of Medicine, 10833 Le Conte Ave., Los Angeles, CA 90095-1747. Phone: (310) 825-1982. Fax: (310)
206-1318. E-mail: uittenbo{at}ucla.edu.
Present address: Division of Clinical Immunology and Allergy,
Children's Hospital Los Angeles, University of Southern California School of Medicine, Los Angeles, Calif.
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