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Research Article Free access | 10.1172/JCI114001

Lymphocyte proliferative responses to human immunodeficiency virus antigens in vitro.

J F Krowka, D P Stites, S Jain, K S Steimer, C George-Nascimento, A Gyenes, P J Barr, H Hollander, A R Moss, and J M Homsy

Department of Laboratory Medicine, University of California, San Francisco 94143-0100.

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Department of Laboratory Medicine, University of California, San Francisco 94143-0100.

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Department of Laboratory Medicine, University of California, San Francisco 94143-0100.

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Department of Laboratory Medicine, University of California, San Francisco 94143-0100.

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Department of Laboratory Medicine, University of California, San Francisco 94143-0100.

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Department of Laboratory Medicine, University of California, San Francisco 94143-0100.

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Published April 1, 1989 - More info

Published in Volume 83, Issue 4 on April 1, 1989
J Clin Invest. 1989;83(4):1198–1203. https://doi.org/10.1172/JCI114001.
© 1989 The American Society for Clinical Investigation
Published April 1, 1989 - Version history
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Abstract

All HIV seronegative (HIV Ab-) and most HIV seropositive (HIV Ab+) individuals' lymphocytes failed to proliferate in primary cultures in response to purified HIV or to recombinant envelope and core antigens of HIV, even in the presence of recombinant interleukin 2 (rIL-2). Most HIV Ab- and HIV Ab+ individuals' lymphocytes, however, could proliferate or be induced by rIL-2 to proliferate in response to lysates of Escherichia coli or Saccharomyces cerevisiae. These findings indicate selective defects in lymphocyte proliferative responses to HIV antigens before the development of AIDS in which lymphocytes are unable to proliferate in response to any antigens. These defects in cell-mediated immune responses to HIV antigens are likely to play an important role in the pathobiology of HIV infections. Although intact HIV or glycosylated gp120 envelope protein of HIV are involved in these defects, a non-glycosylated recombinant form of the HIV gp120 envelope (ENV2-3) and p25 core proteins did not inhibit antigen- or mitogen-driven lymphocyte proliferation.

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