ArticleVirology2007
Antigen stimulation induces HIV envelope gp120-specific CD4(+) T cells to secrete CCR5 ligands and suppress HIV infection.
Article in Virology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 19 citations in OpenAlex.
- Highly dampened HIV-specific cytolytic effector T cell responses define viremic non-progression.Immunobiology · 2022Article
- Differential effects of HIV transmission from monocyte-derived dendritic cells vs. monocytes to IL-17+CD4+ T cells.Journal of leukocyte biology · 2017Article
- Article
- Preferential infection of human Ad5-specific CD4 T cells by HIV in Ad5 naturally exposed and recombinant Ad5-HIV vaccinated individuals.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Preferential HIV infection of CCR6+ Th17 cells is associated with higher levels of virus receptor expression and lack of CCR5 ligands.Journal of virology · 2013Article
- In vitro restoration of Th17 response during HIV infection with an antiretroviral drug and Th17 differentiation cytokines.AIDS research and human retroviruses · 2012Article
- Soluble factors from T cells inhibiting X4 strains of HIV are a mixture of β chemokines and RNases.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- HIV envelope gp120 activates LFA-1 on CD4 T-lymphocytes and increases cell susceptibility to LFA-1-targeting leukotoxin (LtxA).PloS one · 2011Article
- Secretion of MIP-1β and MIP-1α by CD8(+) T-lymphocytes correlates with HIV-1 inhibition independent of coreceptor usage.Cellular immunology · 2011Article
- Clearance of HIV type 1 envelope recombinant sendai virus depends on CD4+ T cells and interferon-gamma but not B cells, CD8+ T cells, or perforin.AIDS research and human retroviruses · 2010Article
- Article
- Stromal cell-derived factor 1 polymorphism in patients infected with HIV and implications for AIDS progression in Tunisia.HIV/AIDS (Auckland, N.Z.) · 2010Article
- Strong ability of Nef-specific CD4+ cytotoxic T cells to suppress human immunodeficiency virus type 1 (HIV-1) replication in HIV-1-infected CD4+ T cells and macrophages.Journal of virology · 2009Article
- Genetic determinants of HIV-1 infection and progression to AIDS: susceptibility to HIV infection.Tissue antigens · 2009Review
Corrections and comments
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Authors and funding
9 authors at 4 institutions in 2 countries.
Funding
Abstract
CD4(+) T cells are critical for effective immune responses against HIV, but they are also the main cell type targeted by the virus. To investigate the key factors that could protect these cells from infection, we evaluated the capacity of HIV gp120-specific human CD4(+) T cells to produce chemokines that inhibit HIV and determined their contribution in suppressing infection in the cells. Antigen stimulation of the CD4(+) T cells elicited production of high amounts of CCR5 chemokines MIP-1alpha (CCL3), MIP-1beta (CCL4), and RANTES (CCL5). Production of these CCR5 ligands was more readily and reproducibly detected than that of IFN-gamma or IL-2. Importantly, in association with secretion of the CCR5 ligands, antigen stimulation made these CD4(+) T cells more resistant to CCR5-tropic HIV-1. Conversely, in the absence of antigen stimulation, the cells were readily infected by the virus, and after infection, their capacity to produce MIP-1beta and IFN-gamma rapidly declined. Thus, vaccines that trigger HIV-specific CD4(+) T cells to elicit robust and rapid production of anti-viral chemokines would be advantageous. Such responses would protect virus-specific CD4(+) T cells from HIV infection and preserve their critical functions in mounting and maintaining long-lasting immunity against the virus.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.