ArticleJournal of virology2011
Kaposi's sarcoma-associated herpesvirus infection of endothelial cells inhibits neutrophil recruitment through an interleukin-6-dependent mechanism: a new paradigm for viral immune evasion.
Article in Journal of virology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
18 citing papers in PubMed, 34 citations in OpenAlex.
- Podocytes regulate neutrophil recruitment by glomerular endothelial cells via IL-6-mediated crosstalk.Journal of immunology (Baltimore, Md. : 1950) · 2014Trial
- Transcriptome and m6A epitranscriptome profiling reveal CCL20 as a key mediator of inflammation in Staphylococcus aureus-induced bovine mastitis.BMC microbiology · 2026Article
- Analysis of tumor infiltrating immune cells in Kaposi sarcoma lesions discovers shifts in macrophage populations.Global health & medicine · 2024Article
- Review
- Cells of the Innate and Adaptive Immune Systems in Kaposi's Sarcoma.Journal of immunology research · 2020Review
- Article
- Infection and immune control of human oncogenic γ-herpesviruses in humanized mice.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2019Review
- SOCS and Herpesviruses, With Emphasis on Cytomegalovirus Retinitis.Frontiers in immunology · 2019Review
- Suppressor of Cytokine Signaling 1 (SOCS1) and SOCS3 Are Stimulated within the Eye during Experimental Murine Cytomegalovirus Retinitis in Mice with Retrovirus-Induced Immunosuppression.Journal of virology · 2018Article
- Bone morphogenetic protein 9 (BMP9) and BMP10 enhance tumor necrosis factor-α-induced monocyte recruitment to the vascular endothelium mainly via activin receptor-like kinase 2.The Journal of biological chemistry · 2017Article
- Monocyte Subsets Coregulate Inflammatory Responses by Integrated Signaling through TNF and IL-6 at the Endothelial Cell Interface.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Bone Morphogenetic Protein 9 Enhances Lipopolysaccharide-Induced Leukocyte Recruitment to the Vascular Endothelium.Journal of immunology (Baltimore, Md. : 1950) · 2016Article
- Immune control of oncogenic γ-herpesviruses.Current opinion in virology · 2015Review
- The effect of environmental chemicals on the tumor microenvironment.Carcinogenesis · 2015Review
- Interplay between Kaposi's sarcoma-associated herpesvirus and the innate immune system.Cytokine & growth factor reviews · 2014Review
- Infection and transmission dynamics of rKSHV.219 in primary endothelial cells.Journal of virological methods · 2013Article
- Human cytomegalovirus induces a biphasic inflammatory response in primary endothelial cells.Journal of virology · 2013Article
- Kaposi's sarcoma-associated herpesvirus inhibits expression and function of endothelial cell major histocompatibility complex class II via suppressor of cytokine signaling 3.Journal of virology · 2012Article
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 2 countries.
Funding
Abstract
Kaposi's sarcoma-associated herpesvirus (KSHV) is the etiological agent of Kaposi's sarcoma (KS), an endothelial cell (EC) neoplasm characterized by dysregulated angiogenesis and inflammation. KSHV infection of EC causes production of proinflammatory mediators, regarded as possible initiators of the substantial mononuclear leukocyte recruitment seen in KS. Conversely, KSHV immune evasion strategies exist, such as degradation of EC leukocyte adhesion receptors by viral proteins. Here, we report the effects of KSHV infection of primary EC on recruitment of flowing leukocytes. Infection did not initiate adhesion of any leukocyte subset per se. However, on cytokine-stimulated EC, KSHV specifically inhibited neutrophil, but not PBL or monocyte, transmigration, an observation consistent with the inflammatory cell profile found in KS lesions in vivo. This inhibition could be recapitulated on uninfected EC using supernatant from infected cultures. These supernatants contained elevated levels of human interleukin 6 (hIL-6), and both the KSHV- and the supernatant-induced inhibitions of neutrophil transmigration were abrogated in the presence of a hIL-6 neutralizing antibody. Furthermore, preconditioning of EC with hIL-6 mimicked the effect of KSHV. Using RNA interference (RNAi), we show that upregulation of suppressor of cytokine signaling 3 (SOCS3) was necessary for this effect of hIL-6. These studies reveal a novel paracrine mode of KSHV immune evasion, resulting in reduced recruitment of neutrophils, a cell type whose antiviral and antitumor roles are becoming increasingly appreciated. Moreover, the findings have implications for our understanding of the contribution of hIL-6 to the pathogenesis of other inflammatory disorders and tumors in which this cytokine is abundant.
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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.