ArticleThe American journal of pathology2001
Murine gammaherpesvirus-68 infection causes multi-organ fibrosis and alters leukocyte trafficking in interferon-gamma receptor knockout mice.
Article in The American journal of pathology, 2001. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 69 citations in OpenAlex.
- Advances in Selenium and Related Compounds Inhibiting Multi-Organ Fibrosis.Drug design, development and therapy · 2025Review
- Article
- Association of tumors having Epstein-Barr virus in surrounding lymphocytes with poor prognosis.Cancer medicine · 2023Article
- Emerging cellular and molecular determinants of idiopathic pulmonary fibrosis.Cellular and molecular life sciences : CMLS · 2021Review
- Control of B Cell Lymphoma by Gammaherpesvirus-Induced Memory CD8 T Cells.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- Hospitalization With Major Infection and Incidence of End-Stage Renal Disease: The Atherosclerosis Risk in Communities (ARIC) Study.Mayo Clinic proceedings · 2020Article
- Genetic Risk Factors for Idiopathic Pulmonary Fibrosis: Insights into Immunopathogenesis.Journal of inflammation research · 2020Review
- Cell Type-Specific Interferon-γ-mediated Antagonism of KSHV Lytic Replication.Scientific reports · 2019Article
- A Human Gain-of-Function STING Mutation Causes Immunodeficiency and Gammaherpesvirus-Induced Pulmonary Fibrosis in Mice.Journal of virology · 2019Article
- Proteomics of Bronchoalveolar Lavage Fluid Reveals a Lung Oxidative Stress Response in Murine Herpesvirus-68 Infection.Viruses · 2018Article
- Inhibition of murine herpesvirus-68 replication by IFN-gamma in macrophages is counteracted by the induction of SOCS1 expression.PLoS pathogens · 2018Article
- Loss of CCR2 signaling alters leukocyte recruitment and exacerbates γ-herpesvirus-induced pneumonitis and fibrosis following bone marrow transplantation.American journal of physiology. Lung cellular and molecular physiology · 2016Article
- The small noncoding RNAs (sncRNAs) of murine gammaherpesvirus 68 (MHV-68) are involved in regulating the latent-to-lytic switch in vivo.Scientific reports · 2016Article
- Viruses in Idiopathic Pulmonary Fibrosis. Etiology and Exacerbation.Annals of the American Thoracic Society · 2015Review
- Effects of Sleep Fragmentation and Chronic Latent Viral Infection on Behavior and Inflammation in Mice.Comparative medicine · 2015Article
- Article
- CD8+ T Cell Response to Gammaherpesvirus Infection Mediates Inflammation and Fibrosis in Interferon Gamma Receptor-Deficient Mice.PloS one · 2015Article
- CD4 T cells specific for a latency-associated γ-herpesvirus epitope are polyfunctional and cytotoxic.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Epstein-Barr virus infection induces aberrant TLR activation pathway and fibroblast-myofibroblast conversion in scleroderma.The Journal of investigative dermatology · 2014Article
- Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Murine gammaherpesvirus-68 (MHV-68) infection in interferon-gamma receptor knockout mice (IFN-gammaR(-)/(-)) results in splenic fibrosis and excessive loss of splenocytes. In our present study we found that MHV-68 infection in IFN-gammaR(-)/(-) mice also resulted in fibrosis and atrophy of the mediastinal lymph nodes, interstitial pulmonary fibrosis and fibrotic changes in the liver. Atrophy and cellular depletion of the spleen in IFN-gammaR(-)/(-) was not the result of increased cell death. The loss of splenocytes in IFN-gammaR(-)/(-) mice, which was most evident on day 23 after infection, correlated with an increase in the number of leukocytes in peripheral blood. At the peak of leukocytosis, on day 23 after infection, peripheral blood cells from infected IFN-gammaR(-)/(-) mice were unable to traffic through the fibrosed spleens of IFN-gammaR(-)/(-) mice but were able to enter the spleens of wild-type mice. This indicates that leukocytosis was in part the result of emigration of cells from the spleen and their subsequent exclusion of re-entry at the height of fibrosis. Significant cytokine and chemokine changes were observed in spleens of IFN-gammaR(-)/(-) mice. IFN-gamma, tumor necrosis factor-alpha (TNF-alpha ), TNF-beta, interleukin-1beta (IL-1beta), transforming growth factor-beta1 (TGF-beta1), lymphotactin, and MIP-1beta were elevated on day 14 after infection whereas chemokines IP-10 and MIG were significantly reduced. These changes suggest a role for dysregulated cytokines and chemokines in severe organ-specific fibrosis with implications for immune-mediated fibrotic disorders.
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