Summary auto-generated
This study examined transforming growth factor β (TGF-β) production during rat cytomegalovirus (RCMV) infection in both immunocompetent and radiation-immunosuppressed rats. The researchers found that splenocytes from infected immunocompetent rats released increased TGF-β1 levels at days 3 and 7 post-infection. In immunosuppressed rats, sera from day 7 infected animals inhibited interleukin-2-induced T cell proliferation, an effect reversible by anti-TGF-β antibodies. Immunohistochemical analysis revealed TGF-β expression in lungs, spleen, liver, and bone marrow stromal cells of infected animals. Importantly, RCMV directly induced TGF-β production in infected fibroblast cultures, as demonstrated by heat-activated supernatants containing TGF-β activity neutralizable by anti-TGF-β antibodies. The TGF-β production coincided with suppressed interleukin-1 bioactivity despite in vitro IL-1 induction. The authors propose that TGF-β production during CMV infection contributes to immunosuppression and pathological changes, including impaired hematopoietic recovery and interstitial pneumonia.
Key findings
- RCMV infection induces elevated TGF-β1 production in splenocytes during acute infection (days 3 and 7 post-infection)
- Sera from infected immunosuppressed rats suppressed T cell proliferation through TGF-β-mediated mechanisms, reversible by neutralizing antibodies
- TGF-β is produced directly by virus-infected cells and localized to bone marrow stromal cells, lungs, liver, and spleen
- TGF-β production coincides with suppression of interleukin-1 bioactivity, suggesting a mechanism for CMV-induced immunosuppression
- Enhanced TGF-β may contribute to CMV pathogenesis through immunosuppression, impaired hematopoiesis, and tissue damage
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Abstract
We analysed the production of transforming growth factor beta (TGF- beta) during a cytomegalovirus (CMV) infection in a rat model system. Splenocytes from immunocompetent rats infected with rat CMV (RCMV) released increased amounts of TGF-beta1. TGF-beta production was also evident in RCMV-infected radiation-immunosuppressed rats; their sera inhibited the interleukin 2-induced proliferation of T cells, which could be restored by anti-TGF-beta antibodies. In addition, TGF-beta production could be visualized immunohistologically in the lungs, spleen, liver and bone marrow of radiation-immunosuppressed infected rats. The virus directly induced this cytokine since TGF-beta was produced upon RCMV infection in vitro. The induction of TGF-beta production may contribute to immunosuppression during CMV infection.