Matches in SemOpenAlex for { <https://semopenalex.org/work/W178672938> ?p ?o ?g. }
- W178672938 endingPage "235" @default.
- W178672938 startingPage "215" @default.
- W178672938 abstract "High-dose chemotherapy (HDT) followed by stem cell transplantation (SCT), using mobilized blood stem cell product (BSCP), cord blood, or bone marrow (BM), is used to treat a variety of advanced malignancies, as well as congenital and autoimmune conditions. In the last decade, it has become apparent that following HDT with an SCT, using either an allogeneic or autologous BSCP, causes more rapid neutrophil, platelet, and immune recoveries to be observed in comparison to an SCT with a BM product. We and others have observed an immune dysfunction in the peripheral blood (PB) of patients following HDT and SCT despite restoration of total T cell numbers. This immunologic dysfunction includes an inversion in the CD4:CD8 T cell ratio and a depression of T cell function. Mechanistic studies have demonstrated a cell-mediated suppression of T cell function in mobilized BSCP and the PB of allogeneic and autologous SCT patients. This loss of function has been associated with increased T cell apoptosis, which occurs predominantly within CD4+ T cell subpopulations. The induction of apoptosis is mediated, at least in part, by Fas Ligand (FasL) expression on monocytes, which are found in significantly higher numbers in mobilized BSCP and in the PB following SCT. In addition, high levels of type 2 cytokines are found in the infused T cells and monocytes as well as in the PB post-transplantation. These defects in immune function may be clinically relevant, as the tolerance induced following HDT and SCT may limit the acute graft-vs-host disease (GVHD) that occurs following the infusion of 10- to 100-fold greater numbers of T cells by an allogeneic mobilized BSCP, as compared to bone marrow transplant trol. CD4+ and CD8+ T cells have been shown to have a pivotal role in controlling the initial infection and maintaining CMV and EBV in a latent state. EBV causes potentially lethal immunoblastic lymphomas in approx 25% of SCT recipients receiving a stem cell product from unrelated or HLA-mismatched donors. Risk factors, which include TCD, major MHCmismatched transplants, and intensity of immunosuppression, support the role of T cell immune surveillance in the control of EBV (188) and CMV infections. CMV pneumonitis (191), despite ganciclovir and specific immunoglobulin therapy, has a poor outcome with a mortality rate of 30–70% (192). Thus, strategies involving the adoptive transfer of CMV- or EBVspecific CTL clones or boosting of donor or patient immunity using CMV or EBV vaccines are encouraging. If the allo-donor is vaccinated, the T cells contained within the stem cell product include, in theory, viral-specific CTL. Alternatively, CTL may be derived following ex vivo-expansion of virus-specific CTL using donor leukocytes. In either case, the leukocytes or isolated T cells can be given either prophylactically or therapeutically for the treatment of CMV and EBV infections. The EBV-specific CTL are readily stimulated and expanded using EBV-immortalized B lymphoblastoid cell lines as stimulators. Current protocols for CMVspecific CTL use transfection of PP65, an immunodominant CMV antigen into CMV-infected fibroblasts, DCs or EBV-transformed B lymphoblastic cell lines and used for antigen stimulation (186). Thus, graft manipulation via antigen-specific T cell augmentation, either ex vivo or by donor vaccination, has significant potential as a strategy to affect infection. Further, the utilization of DLI from vaccinated donors or ex vivo-stimulated and expanded viral-specific CTLs provides an exciting new strategy for the control of these life-threatening viral infections (186). Regardless of the strategy used to prevent or treat infections, the marked and prolonged cellular immunodeficiency that is observed following SCT—especially following transplantation with positively selected stem cells—results in an increased incidence of infections, including rare and unusual infections, such as Pneumocystis carinii, toxoplasmosism and Mycobacterium species." @default.
- W178672938 created "2016-06-24" @default.
- W178672938 creator A5089092786 @default.
- W178672938 date "2003-01-01" @default.
- W178672938 modified "2023-09-24" @default.
- W178672938 title "Immune Recovery Following Allogeneic Blood Transplantation" @default.
- W178672938 cites W137159086 @default.
- W178672938 cites W148001558 @default.
- W178672938 cites W1537330558 @default.
- W178672938 cites W1539005347 @default.
- W178672938 cites W1539984014 @default.
- W178672938 cites W1558647085 @default.
- W178672938 cites W1571009995 @default.
- W178672938 cites W1572649987 @default.
- W178672938 cites W1579000294 @default.
- W178672938 cites W1580217007 @default.
- W178672938 cites W1594245074 @default.
- W178672938 cites W1594989289 @default.
- W178672938 cites W1604668557 @default.
- W178672938 cites W1615239198 @default.
- W178672938 cites W168192535 @default.
- W178672938 cites W1683467081 @default.
- W178672938 cites W1737344958 @default.
- W178672938 cites W1842423069 @default.
- W178672938 cites W190201512 @default.
- W178672938 cites W1934677454 @default.
- W178672938 cites W1947598746 @default.
- W178672938 cites W1963688949 @default.
- W178672938 cites W1964964271 @default.
- W178672938 cites W1965974612 @default.
- W178672938 cites W1970447682 @default.
- W178672938 cites W1970529772 @default.
- W178672938 cites W1972758309 @default.
- W178672938 cites W1974393084 @default.
- W178672938 cites W1977635228 @default.
- W178672938 cites W1980785340 @default.
- W178672938 cites W1981668042 @default.
- W178672938 cites W1983858501 @default.
- W178672938 cites W1983916012 @default.
- W178672938 cites W1985585224 @default.
- W178672938 cites W1987359936 @default.
- W178672938 cites W1987968353 @default.
- W178672938 cites W1988749990 @default.
- W178672938 cites W1991756452 @default.
- W178672938 cites W1999463201 @default.
- W178672938 cites W1999478930 @default.
- W178672938 cites W2000498898 @default.
- W178672938 cites W2002507218 @default.
- W178672938 cites W2002733542 @default.
- W178672938 cites W2003285575 @default.
- W178672938 cites W2004645606 @default.
- W178672938 cites W2006295168 @default.
- W178672938 cites W2010018874 @default.
- W178672938 cites W2010033272 @default.
- W178672938 cites W2014779265 @default.
- W178672938 cites W2014859281 @default.
- W178672938 cites W2016857765 @default.
- W178672938 cites W2019046456 @default.
- W178672938 cites W2019291297 @default.
- W178672938 cites W2019522474 @default.
- W178672938 cites W2020400573 @default.
- W178672938 cites W2022090978 @default.
- W178672938 cites W2023122026 @default.
- W178672938 cites W2030448629 @default.
- W178672938 cites W2030455150 @default.
- W178672938 cites W2030952613 @default.
- W178672938 cites W2031416111 @default.
- W178672938 cites W2034213207 @default.
- W178672938 cites W2036026019 @default.
- W178672938 cites W2036300571 @default.
- W178672938 cites W2039414848 @default.
- W178672938 cites W2040226771 @default.
- W178672938 cites W2040735196 @default.
- W178672938 cites W2042371846 @default.
- W178672938 cites W2044092330 @default.
- W178672938 cites W2048457755 @default.
- W178672938 cites W2048526870 @default.
- W178672938 cites W2049463886 @default.
- W178672938 cites W2050642909 @default.
- W178672938 cites W2053124731 @default.
- W178672938 cites W2054076339 @default.
- W178672938 cites W2058935272 @default.
- W178672938 cites W2060524822 @default.
- W178672938 cites W2063116616 @default.
- W178672938 cites W2064579091 @default.
- W178672938 cites W2066128121 @default.
- W178672938 cites W2066684881 @default.
- W178672938 cites W2069987316 @default.
- W178672938 cites W2071360821 @default.
- W178672938 cites W2076002999 @default.
- W178672938 cites W2076597201 @default.
- W178672938 cites W2077718766 @default.
- W178672938 cites W2079149944 @default.
- W178672938 cites W2080990010 @default.
- W178672938 cites W2084886561 @default.
- W178672938 cites W2086313080 @default.
- W178672938 cites W2088895543 @default.
- W178672938 cites W2091704657 @default.