ArticlePloS one2013
HSV-2 regulates monocyte inflammatory response via the Fas/FasL pathway.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It carries an expression of concern. Cited by 18 papers.
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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
18 citing papers in PubMed, 27 citations in OpenAlex.
- Expression of concern: HSV-2 regulates monocyte inflammatory response via the Fas/FasL pathway.PloS one · 2026Article
- FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025Review
- Fas/FasL-Mediated Apoptosis and Inflammation Contribute to Recovery from HSV-2-Mediated Spinal Cord Infection.Viruses · 2024Article
- Apoptotic cell death in disease-Current understanding of the NCCD 2023.Cell death and differentiation · 2023Review
- Human herpesvirus type 2 infection of primary murine astrocytes causes disruption of the mitochondrial network and remodeling of the actin cytoskeleton: an in vitro morphological study.Archives of virology · 2021Article
- Defining the Innate Immune Responses for SARS-CoV-2-Human Macrophage Interactions.Frontiers in immunology · 2021Article
- Fas/FasL Contributes to HSV-1 Brain Infection and Neuroinflammation.Frontiers in immunology · 2021Article
- Immunoregulatory Functions of Interferons During Genital HSV-2 Infection.Frontiers in immunology · 2021Review
- Disturbances of mitochondrial dynamics in cultured neurons infected with human herpesvirus type 1 and type 2.Journal of neurovirology · 2019Article
- HBV and HIV/HBV Infected Patients Have Distinct Immune Exhaustion and Apoptotic Serum Biomarker Profiles.Pathogens & immunity · 2019Article
- Nitric Oxide Influences HSV-1-Induced Neuroinflammation.Oxidative medicine and cellular longevity · 2019Article
- Human herpesvirus type 1 and type 2 disrupt mitochondrial dynamics in human keratinocytes.Archives of virology · 2018Article
- Virus Infection and Death Receptor-Mediated Apoptosis.Viruses · 2017Review
- Involvement of Fas/FasL pathway in the murine model of atopic dermatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2017Article
- IL-36γ Augments Host Defense and Immune Responses in Human Female Reproductive Tract Epithelial Cells.Frontiers in microbiology · 2016Article
- Fas/FasL pathway participates in regulation of antiviral and inflammatory response during mousepox infection of lungs.Mediators of inflammation · 2015Article
- Engagement of Fas on Macrophages Modulates Poly I:C induced cytokine production with specific enhancement of IP-10.PloS one · 2015Article
- Herpes simplex virus type-2 stimulates HIV-1 replication in cervical tissues: implications for HIV-1 transmission and efficacy of anti-HIV-1 microbicides.Mucosal immunology · 2014Article
Corrections and comments
- Expression of concern
Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Monocytic cells represent important cellular elements of the innate and adaptive immune responses in viral infections. We assessed the role of Fas/FasL in promoting monocyte apoptosis during HSV-2 infection by using an in vitro model based on the murine RAW 264.7 monocytic cell line and an in vivo murine model of HSV-2 infection applied to C57BL6, MRL-Fas(lpr)/J (Fas-/-) and C3-Fasl(gld)/J (FasL-/-) mice. HSV-2 infection of the monocytic cell line led to early induction of apoptosis, with no protective expression of anti-apoptotic Bcl-2. HSV-2 infected monocytes up-regulated Fas and FasL expression early during in vitro infection but were susceptible to Fas induced apoptosis. The vaginal monocytes in the HSV-2 murine model of infection up-regulated FasL expression and were susceptible to Fas induced apoptosis. HSV-2 infection of Fas and FasL- deficient mice led to decreased apoptosis of monocytes and impaired recruitment of NK, CD4+ and CD8+ T cells within the infection sites. The vaginal lavages of HSV-2 infected Fas and FasL- deficient showed decreased production of CXCL9, CXCL10 and TNF-α in comparison to HSV-2 infected wild-type mice strain. The decreased recruitment of immune competent cells was accompanied by delayed virus clearance from the infected tissue. Triggering of the Fas receptor on HSV-2 infected monocytes in vitro up-regulated the expression of CXCL9 chemokines and the cytokine TNF-α. Our study provides novel insights on the role of Fas/FasL pathway not only in apoptosis of monocytes but also in regulating local immune response by monocytes during HSV-2 infection.
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