期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 110, 期 22, 页码 9019-9024出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1301456110
关键词
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资金
- Center for HIV/AIDS Vaccine Immunology (CHAVI)-Immunogen Discovery Grant [U01 AI067854]
- National Institutes of Health, National Institute of Allergy and Infectious Diseases Division of Acquired Immunodeficiency Syndrome (NIH/NIAID/DAIDS)
- NIH NIAID [AI07392]
- Bill and Melinda Gates Foundation [1033098, 1040758]
- Collaboration for AIDS Vaccine Discovery-Vaccine Immune Monitoring Consortium (CAVD-VIMC) Grant [3830913]
- CAVD-VIMC Grant [CTVIMC OPP1032325]
- HIV-1 Vaccine Trials Network [5U01 AI46725-05]
- Duke University Center for AIDS Research [P30 AI64518]
- US Army Medical Research and Material Command [Y1-AI-2642-12]
- NIAID [Y1-AI-2642-12, W81XWH-07-2-0067]
- Henry M. Jackson Foundation for the Advancement of Military Medicine, Inc.
- US Department of Defense
Analysis of correlates of risk of infection in the RV144 HIV-1 vaccine efficacy trial demonstrated that plasma IgG against the HIV-1 envelope (Env) variable region 1 and 2 inversely correlated with risk, whereas HIV-1 Env-specific plasma IgA responses directly correlated with risk. In the secondary analysis, antibody-dependent cellular cytotoxicity (ADCC) was another inverse correlate of risk, but only in the presence of low plasma IgA Env-specific antibodies. Thus, we investigated the hypothesis that IgA could attenuate the protective effect of IgG responses through competition for the same Env binding sites. We report that Env-specific plasma IgA/IgG ratios are higher in infected than in uninfected vaccine recipients in RV144. Moreover, Env-specific IgA antibodies from RV144 vaccinees blocked the binding of ADCC-mediating mAb to HIV-1 Env glycoprotein 120 (gp120). An Env-specific monomeric IgA mAb isolated from an RV144 vaccinee also inhibited the ability of natural killer cells to kill HIV-1-infected CD4(+) T cells coated with RV144-induced IgG antibodies. We show that monomeric Env-specific IgA, as part of postvaccination polyclonal antibody response, may modulate vaccine-induced immunity by diminishing ADCC effector function.
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