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Titlebook: Gene Therapy in Inflammatory Diseases; Christopher H. Evans,Paul D. Robbins Book 2000 Springer Basel AG 2000 Arthritis.DNA.apoptosis.carti

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樓主: 爆發(fā)
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發(fā)表于 2025-3-26 22:56:57 | 只看該作者
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發(fā)表于 2025-3-27 03:07:32 | 只看該作者
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Gene therapy for type I diabetes mellitus,ther loci have subsequently been identified using whole genome scanning approaches in affected sib-pair linkage analyses; however, the association of many of these loci to IDDM has recently been questioned [5–8]. It must be borne in mind that the genetic transmission of susceptibility alleles at loc
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發(fā)表于 2025-3-27 18:55:02 | 只看該作者
Gene transfer to facilitate transplantation, for the most part involves responses to non-MHC antigens. Functional consequences of these differences are that MHC antigens can be presented directly to class I or class II allorestricted CD8. or CD4. T cells, respectively, or processed MHC-derived peptides can be represented indirectly to self-re
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發(fā)表于 2025-3-28 01:55:30 | 只看該作者
Book 2000atment of an inflammatory disease. As well as providing novel therapeutic approaches, gene therapy facilitates the development of new and improved animal models of disease; a chapter describing these advances is also included. As an up-to-date, timely book written by th
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R. Delanghe,F. Sommen,V. Sou?ek identified that play a role in this process. Further investigations of Fas/FasL regulation should allow development of strategies to restore T-cell tolerance in autoimmune situations. In this chapter, we shall describe potential applications of gene therapy to develop strategies to overcome these d
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