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Research Article Free access | 10.1172/JCI114090
Laboratory for Acquired Immunodeficiency Syndrome (AIDS) Virus Research, Hospital for Special Surgery, New York.
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Laboratory for Acquired Immunodeficiency Syndrome (AIDS) Virus Research, Hospital for Special Surgery, New York.
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Laboratory for Acquired Immunodeficiency Syndrome (AIDS) Virus Research, Hospital for Special Surgery, New York.
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Laboratory for Acquired Immunodeficiency Syndrome (AIDS) Virus Research, Hospital for Special Surgery, New York.
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Laboratory for Acquired Immunodeficiency Syndrome (AIDS) Virus Research, Hospital for Special Surgery, New York.
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Published June 1, 1989 - More info
HIV selectively inhibited the proliferative response of clonal CD4+ T lymphocytes to alloantigen while other alloantigen-dependent responses were unperturbed. Specifically, impaired blastogenesis could be dissociated from alloantigen-specific induction of the B cell activation molecule CD23, IL-4 release, and inositol lipid hydrolysis. In addition, membrane expression of pertinent T cell receptor molecules, including CD2, CD3, and T cell antigen receptor (Ti), remained intact. Using two MHC class II-specific human CD4+ helper T cell clones, the proliferative defect was shown to be an early consequence of HIV infection, occurring within 4 d of viral inoculation and preceding increases in mature virion production. It was generalizable to three distinct methods of T cell activation, all independent of antigen-presenting cells: anti-CD3 mediated cross-linking of the CD3/Ti complex; anti-CD2 and phorbol 12-myristic 13-acetate (PMA); and anti-CD28 plus PMA. These abnormalities were not mitigated by addition of exogenous IL-2, even though expression of the IL-2 receptor (CD25) was unaltered. These studies define a selective blockade in T cell function early after HIV exposure that could serve as a model for certain in vivo manifestations of AIDS.