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Role of NKT cells in allogeneic islet graft survival
Cited 20 time in
Web of Science
Cited 20 time in Scopus
- Authors
- Issue Date
- 2007-07-31
- Publisher
- Elsevier
- Citation
- Clin Immunol. 2007 Sep;124(3):258-66. Epub 2007 Jul 26.
- Keywords
- Animals ; Antigens, CD1/genetics/*metabolism ; Antigens, CD1d ; Graft Survival/*immunology ; Histocompatibility Antigens Class II/metabolism ; Islets of Langerhans Transplantation/*immunology ; Killer Cells, Natural/*immunology ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Time Factors ; Transforming Growth Factor beta/metabolism ; Transplantation Tolerance/immunology ; Up-Regulation
- Abstract
- Although NKT cells expressing CD1d-reactive TCR exerted protective role in autoimmune diseases, the regulatory function of CD1d-dependent NKT cells in alloimmune responses has not been investigated thoroughly. Here, we demonstrated the regulatory effects of NKT cells using a pancreas islet transplantation model. CD40/CD154 blocking induced long-term graft survival in most B6 recipients, but B6.CD1d(-/-) recipients showed co-stimulation blockade-resistant rejection. Adoptive transfer of NKT cells into B6.CD1d(-/-) restored tolerizing capacity of co-stimulatory blockade. Activation of NKT cells was effective for the prolongation of graft survival and up-regulated membrane-bound TGF-beta expression transiently on their cell surface. The activated CD1d-dependent NKT cells inhibited alloantigen-driven cell proliferation through cell contacts and the beneficial effect of CD154 blocking for allograft survival was related to TGF-beta pathway. Thus, we can conclude that NKT cells are essential for the stable allograft survival and the regulatory function is dependent on, at least in part, TGF-beta engagement.
- ISSN
- 1521-6616 (Print)
- Language
- English
- URI
- http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&dopt=Citation&list_uids=17662658
https://hdl.handle.net/10371/24100
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