ArticleClinical and experimental immunology1998
Recombinant human IL-16 inhibits HIV-1 replication and protects against activation-induced cell death (AICD).
Article in Clinical and experimental immunology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 41 citations in OpenAlex.
- Cytokine expression in the colonic mucosa of human immunodeficiency virus-infected individuals before and during 9 months of antiretroviral therapy.Antimicrobial agents and chemotherapy · 2008Trial
- An eQTL-based approach reveals candidate regulators of LINE-1 RNA levels in lymphoblastoid cells.PLoS genetics · 2024Article
- An eQTL-based Approach Reveals Candidate Regulators of LINE-1 RNA Levels in Lymphoblastoid Cells.bioRxiv : the preprint server for biology · 2023Article
- The CD8Microbiology and molecular biology reviews : MMBR · 2021Review
- Secondary necrotic neutrophils release interleukin-16C and macrophage migration inhibitory factor from stores in the cytosol.Cell death discovery · 2015Article
- The synthetic immunomodulator murabutide controls human immunodeficiency virus type 1 replication at multiple levels in macrophages and dendritic cells.Journal of virology · 2000Article
- Interleukin-16 stimulates the expression and production of pro-inflammatory cytokines by human monocytes.Immunology · 2000Article
- Interleukin-16 inhibits human immunodeficiency virus type 1 entry and replication in macrophages and in dendritic cells.Journal of virology · 1999Article
- Recombinant interleukin-16 selectively modulates surface receptor expression and cytokine release in macrophages and dendritic cells.Immunology · 1999Article
- GA-binding protein factors, in concert with the coactivator CREB binding protein/p300, control the induction of the interleukin 16 promoter in T lymphocytes.Proceedings of the National Academy of Sciences of the United States of America · 1999Article
Corrections and comments
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Authors and funding
8 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The chemoattractant cytokine IL- 16 has been reported to suppress lymphocyte activation and to inhibit HIV-1 replication in acutely infected T cells. We have cloned and expressed human IL-16 in Escherichia coli and investigated whether the recombinant protein could regulate the level of lymphocyte apoptosis from HIV-1-infected subjects. After purification and refolding, only 2-10% of the recombinant cytokine was present in a biologically active homotetrameric form. This could explain the need for high concentrations of the bacterially derived IL- 16 to induce significant inhibition of HIV-1 replication. Addition of IL-16 to unstimulated peripheral blood mononuclear cell (PBMC) cultures from HIV-1-infected subjects did not modify the observed level of spontaneous lymphocyte apoptosis. In contrast, IL-16 added to PBMC cultures stimulated with anti-CD3, anti-CD95 or dexamethasone reduced significantly the percentage of lymphocytes undergoing AICD. This effect was found to correlate with the ability of the cytokine to decrease CD95 expression on activated CD4+ T cells. Comparative studies on PBMC from healthy individuals indicated that the regulation of apoptosis levels by IL-16 is a complex phenomenon and could depend on the nature of the activator used and/or the immune status of lymphocytes tested. The outcome of CD4 cross-linking on T cells by various ligands is discussed in the context of the observed beneficial activities of IL- 16 and its potential role in the treatment of HIV disease.
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