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- W1489663451 abstract "Therapies that control largely T cell-dependent allograft rejection in humans also possess the undesirable effect of impairing T cell function, leaving transplant recipients susceptible to opportunistic viruses. Prime among these opportunists are the ubiquitous herpesviruses. To date, studies are lacking that address the effect of viruses that establish a true latent state on allograft tolerance or the effect of tolerance protocols on the immune control of latent viruses. By using a mixed chimerism-based tolerance-induction protocol, we found that mice undergoing latent infection with gammaHV68, a murine gamma-herpesvirus closely related to human gamma-herpesviruses such as EBV and Kaposi's sarcoma-associated herpesvirus, significantly resist tolerance to allografts. Limiting the degree of virus reactivation or innate immune response did not reconstitute chimerism in latently infected mice. However, gammaHV68-infected mice showed increased frequency of CD8+ T cell alloreactivity and, interestingly, expansion of virus-induced, alloreactive, effector/effector memory TCR Vbeta4+CD8+ T cells driven by the gammaHV68-M1 gene was associated with resistance to tolerance induction in studies using gammaHV68-M1 mutant virus. These results define the viral gene and immune cell types involved in latent infection-mediated resistance to allograft tolerance and underscore the influence of latent herpesviruses on allograft survival." @default.
- W1489663451 created "2016-06-24" @default.
- W1489663451 creator A5016561426 @default.
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- W1489663451 date "2008-03-01" @default.
- W1489663451 modified "2023-09-25" @default.
- W1489663451 title "Expansion of Effector Memory TCR Vβ4+CD8+ T Cells Is Associated with Latent Infection-Mediated Resistance to Transplantation Tolerance" @default.
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- W1489663451 doi "https://doi.org/10.4049/jimmunol.180.5.3190" @default.
- W1489663451 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/18292543" @default.