S-Space College of Medicine/School of Medicine (의과대학/대학원) Internal Medicine (내과학전공) Journal Papers (저널논문_내과학전공)
Role of NKT cells in allogeneic islet graft survival
- Yang, Seung Hee; Jin, Ji Zhe; Lee, Se Han; Park, Hyungbae; Kim, Chi Hwa; Lee, Dong-Sup; Kim, Suhnggwon; Chung, Nam Hyun; Kim, Yon Su
- Issue Date
- Clin Immunol. 2007 Sep;124(3):258-66. Epub 2007 Jul 26.
- 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
- 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.
- 1521-6616 (Print)
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