Sera from HTLV-III/LAV antibody-positive individuals mediate antibody- dependent cellular cytotoxicity against HTLV-III/LAV-infected T cells

The causative agent of the acquired immunodeficiency syndrome (AIDS) has been shown to be a human retrovirus called human T lymphotropic virus (HTLV)-III or lymphadenopathy-associated virus (LAV). The nature of the protective immune response against this virus is currently unknown. We report here re...

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Published inThe Journal of immunology (1950) Vol. 138; no. 4; pp. 1064 - 1067
Main Authors Rook, AH, Lane, HC, Folks, T, McCoy, S, Alter, H, Fauci, AS
Format Journal Article
LanguageEnglish
Published Bethesda, MD Am Assoc Immnol 15.02.1987
American Association of Immunologists
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ISSN0022-1767
1550-6606
DOI10.4049/jimmunol.138.4.1064

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Summary:The causative agent of the acquired immunodeficiency syndrome (AIDS) has been shown to be a human retrovirus called human T lymphotropic virus (HTLV)-III or lymphadenopathy-associated virus (LAV). The nature of the protective immune response against this virus is currently unknown. We report here results using an antibody-dependent cellular cytotoxicity (ADCC) assay which has been developed for measuring a specific immune response against HTLV-III/LAV. Forty-four sera were examined for their ability to mediate ADCC against HTLV-III/LAV-infected T cells. Sera from healthy HTLV-III/LAV seropositive individuals in the presence of mononuclear cells from healthy HTLV-III/LAV seronegative donors exhibited significantly higher levels of ADCC activity compared to sera from patients with AIDS. Western blot analysis of serum samples indicated that antibody reactivity with the p24 protein of HTLV-III/LAV correlated with higher levels of ADCC activity than did reactivity with Gp120/160. The observation that sera from healthy HTLV-III/LAV seropositive individuals mediated higher levels of ADCC activity than did sera obtained from subjects with AIDS suggests that ADCC may represent a protective immune response to infection with HTLV-III/LAV.
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ISSN:0022-1767
1550-6606
DOI:10.4049/jimmunol.138.4.1064