CD8+ T cells from healthy blood bank donors secrete antiviral levels of interferon-alpha
| Autor: | M. Scott Killian, Abby Wegehaupt, Ellen Roufs |
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| Rok vydání: | 2017 |
| Předmět: | |
| Zdroj: | The Journal of Immunology. 198:125.6-125.6 |
| ISSN: | 1550-6606 0022-1767 |
| DOI: | 10.4049/jimmunol.198.supp.125.6 |
| Popis: | Background CD8+ T cells play important roles in the antiviral immune response to HIV-1 infection. Variation in the antiviral activities of CD8+ T cells among HIV-1-infected persons has been associated with disease state and clinical prognosis. However, the anti-HIV activities of CD8+ T cells from healthy uninfected blood donors have not been fully established. Methods In this study we assessed the ability of peripheral blood CD8+ T cells from healthy blood bank donors to inhibit HIV-1-replication. Co-culture assays were performed with CD8+ T cells and acutely HIV-1-infected primary CD4+ T cells. Also, CD8+ T cells were cultured and the derivative supernatants were evaluated in virus inhibition assays, ELISAs, and multiplex cytokine arrays. Results Variation was observed among CD8+ T cells from different blood donors in the ability to suppress HIV-1 replication. In the absence of stimulation, the CD8+ T cells, or their derivative fluids, lacked any appreciable anti-HIV activity. After PHA or anti-CD3/CD28 stimulation, the majority of CD8+ T cells and derivative fluids exhibited anti-HIV activity. Low levels of interferon-alpha were present in the CD8+ T cell fluids having increased anti-HIV activity, whereas CD8+ T cell fluids lacking anti-HIV activity contained undetectable levels of interferon-alpha. Other soluble factors present at increased levels in CD8+ T cell fluids having anti-HIV activity included TNF-beta, IL-8, IP-10, and TRAIL. Conclusions Our findings indicate that the secretion of antiviral levels of interferon-alpha is a normal function of CD8+ T cells in response to activation and stimulation. Variation in this immune response may influence host susceptibility to infection and disease. |
| Databáze: | OpenAIRE |
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