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• W2022109398 abstract "Long-term acceptance of MHC-incompatible organ allografts without chronic immunosuppressive therapy has been achieved in experimental animals. There are also reports, mainly in liver transplant, of patients who after complete withdrawal of immunosuppressants still have a functioning graft. It has been proposed that organ transplant implies a migratory flux of donor “passenger” leukocytes out of the graft into the recipient tissues or organs, serving to establish a persistent condition of “microchimerism,” and being a tolerogenic precursor of chimeric cells. Although there is evidence that the same migratory mechanisms apply to all organ grafts, migration of passenger leukocytes is less in organs other than the liver, such as the kidney and heart. To enhance the acceptance of organs less tolerogenic than the liver, perioperative infusion of donor bone marrow has been attempted to increase the migration of donor leukocytes of bone marrow origin. It has been suggested that such peripheral donor microchimerism is not only associated with long-term acceptance of the organ graft but that it plays an active role in induction and maintenance of unresponsiveness. However, the intimate mechanisms(s) responsible for prolonged organ survival in this setting remains speculative. Experimental evidence that the thymus plays the major role in the development of self-tolerance and is also critical in the induction of acquired tolerance to exogenous antigens has focussed the attention on the intrathymic events that lead to donor-specific unresponsiveness to allograft. Data are available showing that after direct intrathymic injection of donor cells, clonal deletion of maturing host thymocytes occurs and is the major mechanism in the induction of donor-specific tolerance. The central role of the thymus in transplant tolerance is also supported by more recent findings that in mixed allogeneic bone marrow chimeras in mice with a nonmyeloablative conditioning regimen, migration of donor bone marrow-derived dendritic cells to the thymus serves to negatively select newly developing host T cells. Therefore, the peripheral T-cell component would be devoid of alloreactive population. Thus, lifelong intrathymic clonal deletion is the only significant mechanism involved in the maintenance of donor-specific T- cell tolerance that would allow the subsequent vascularized organ from the same donor to survive indefinitely. (Am J Kidney Dis 1998 Feb;31(2):197-212)" @default.
• W2022109398 created "2016-06-24" @default.
• W2022109398 creator A5023556434 @default.
• W2022109398 date "1998-02-01" @default.
• W2022109398 modified "2023-10-18" @default.
• W2022109398 title "Cellular basis of long-term organ transplant acceptance: Pivotal role of intrathymic clonal deletion and thymic dependence of bone marrow microchimerism-associated tolerance" @default.
• W2022109398 cites W117988946 @default.
• W2022109398 cites W1520847221 @default.
• W2022109398 cites W153969595 @default.
• W2022109398 cites W1583694308 @default.
• W2022109398 cites W1894844674 @default.
• W2022109398 cites W1965239953 @default.
• W2022109398 cites W1966957841 @default.
• W2022109398 cites W1967891950 @default.
• W2022109398 cites W1970198698 @default.
• W2022109398 cites W1974280847 @default.
• W2022109398 cites W1975063479 @default.
• W2022109398 cites W1981748732 @default.
• W2022109398 cites W1983215753 @default.
• W2022109398 cites W1983329640 @default.
• W2022109398 cites W1985521658 @default.
• W2022109398 cites W1986654358 @default.
• W2022109398 cites W1987508243 @default.
• W2022109398 cites W1989575051 @default.
• W2022109398 cites W1990046941 @default.
• W2022109398 cites W1992611128 @default.
• W2022109398 cites W1996092626 @default.
• W2022109398 cites W2001612209 @default.
• W2022109398 cites W2003204592 @default.
• W2022109398 cites W2004275733 @default.
• W2022109398 cites W2007362831 @default.
• W2022109398 cites W2018848687 @default.
• W2022109398 cites W2018929753 @default.
• W2022109398 cites W2019522474 @default.
• W2022109398 cites W2020873431 @default.
• W2022109398 cites W2023703038 @default.
• W2022109398 cites W2033259350 @default.
• W2022109398 cites W2035135369 @default.
• W2022109398 cites W2035394206 @default.
• W2022109398 cites W2039801541 @default.
• W2022109398 cites W2042689607 @default.
• W2022109398 cites W2048070434 @default.
• W2022109398 cites W2052238968 @default.
• W2022109398 cites W2052360575 @default.
• W2022109398 cites W2067996571 @default.
• W2022109398 cites W2071876985 @default.
• W2022109398 cites W2073113705 @default.
• W2022109398 cites W2074150726 @default.
• W2022109398 cites W2076020359 @default.
• W2022109398 cites W2080883834 @default.
• W2022109398 cites W2082754049 @default.
• W2022109398 cites W2085366465 @default.
• W2022109398 cites W2089951057 @default.
• W2022109398 cites W2100215924 @default.
• W2022109398 cites W2106951989 @default.
• W2022109398 cites W2111135134 @default.
• W2022109398 cites W2112002732 @default.
• W2022109398 cites W2115618940 @default.
• W2022109398 cites W2117889341 @default.
• W2022109398 cites W2128180128 @default.
• W2022109398 cites W2150841203 @default.
• W2022109398 cites W2152553677 @default.
• W2022109398 cites W2152918507 @default.
• W2022109398 cites W2162016426 @default.
• W2022109398 cites W2166948911 @default.
• W2022109398 cites W2177327503 @default.
• W2022109398 cites W2266477885 @default.
• W2022109398 cites W2336171903 @default.
• W2022109398 cites W2405246499 @default.
• W2022109398 cites W2406492414 @default.
• W2022109398 cites W2406717473 @default.
• W2022109398 cites W2410296581 @default.
• W2022109398 cites W2415281201 @default.
• W2022109398 cites W2417850406 @default.
• W2022109398 cites W2418796872 @default.
• W2022109398 cites W2443977771 @default.
• W2022109398 cites W245016890 @default.
• W2022109398 cites W2467014890 @default.
• W2022109398 cites W2469378041 @default.
• W2022109398 cites W2474816364 @default.
• W2022109398 cites W2764895986 @default.
• W2022109398 cites W287984089 @default.
• W2022109398 cites W57310574 @default.
• W2022109398 cites W590753586 @default.
• W2022109398 cites W639804678 @default.
• W2022109398 cites W2396044391 @default.
• W2022109398 doi "https://doi.org/10.1053/ajkd.1998.v31.pm9469488" @default.
• W2022109398 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9469488" @default.
• W2022109398 hasPublicationYear "1998" @default.
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