PubMed · 12559887
The source did not provide an abstract. Follow the original record for more information.
Explore connections, maps & timelines
Atholl Johnston, Gary A Levy. 2003-01-25. The TMC study.. https://doi.org/10.1016/s0140-6736(03)12347-1
Cite the original work for its findings. Save a collection to share your selection of sources.
KEEP EXPLORING
BACKGROUND: Donor-derived, ex vivo-expanded cytotoxic T lymphocytes (CTL) can provide stem-cell transplantation (SCT) patients with a renewed capacity for virus-specific immune surveillance. Because SCT patients are often treated with cyclosporine (CsA), we questioned whether ex vivo-expanded CTL were susceptible to inhibition by this immunosuppressive drug. METHODS: Human Epstein-Barr virus (EBV)-specific CTL were established by cultivating T cells for at least 5 weeks with interleukin (IL)-2 and irradiated, autologous EBV-transformed B-lymphoblastoid cell lines (LCL). In some cases, CsA was added during the last week of T-cell expansion. Effectors were then tested for cytotoxicity toward their targets in a chromium-release assay or by coculture with viable, unlabeled targets, in the presence or absence of CsA. Alloreactive CTL were similarly expanded and tested against major histocompatibility complex-mismatched stimulator cells. RESULTS: CsA had a marginal effect on CTL function when added at concentrations greater than or equal to 250 ng/mL during the 4- to 6-hour chromium release assay. However, exposure of CTL to CsA for 1 week before assay reduced lytic function significantly. When the CTL lines were cocultured with viable targets in the presence of CsA, effectors were unable to eliminate their targets, which ultimately dominated the culture. CONCLUSIONS: We suggest that the activity of ex vivo-expanded CTL may be significantly compromised in the presence of high-dose CsA in vivo, particularly if CTL are administered for the purpose of long-term virus-specific immune surveillance.
Explore the source record for details and available documents.
The increasing use of cyclosporine A (CSA) in organ transplants and in the treatment of autoimmune diseases has increased the incidence of cyclosporine A-related adverse effects, including gingival hyperplasia (GH). GH causes esthetic, speech, mastication and tooth growth problems in the affected patients. The prevalence of cyclosporine-induced GH varies in different studies and may be as high as 85%, depending on the diagnostic criteria. This review approaches etiological, histological and clinical issues, as well as the prevention and treatment of this important injury.