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Transplant Tolerance to Pancreatic Islets Is Initiated in the Graft and Sustained in the Spleen
Transplant Tolerance to Pancreatic Islets Is Initiated in the Graft and Sustained in the Spleen AMERICAN JOURNAL OF TRANSPLANTATION Gagliani, N., Jofra, T., Valle, A., Stabilini, A., Morsiani, C., Gregori, S., Deng, S., Rothstein, D. M., Atkinson, M., Kamanaka, M., Flavell, R. A., Roncarolo, M. G., Battaglia, M. 2013; 13 (8): 1963-1975Abstract
The immune system is comprised of several CD4(+) T regulatory (Treg) cell types, of which two, the Foxp3(+) Treg and T regulatory type 1 (Tr1) cells, have frequently been associated with transplant tolerance. However, whether and how these two Treg-cell types synergize to promote allograft tolerance remains unknown. We previously developed a mouse model of allogeneic transplantation in which a specific immunomodulatory treatment leads to transplant tolerance through both Foxp3(+) Treg and Tr1 cells. Here, we show that Foxp3(+) Treg cells exert their regulatory function within the allograft and initiate engraftment locally and in a non-antigen (Ag) specific manner. Whereas CD4(+) CD25(-) T cells, which contain Tr1 cells, act from the spleen and are key to the maintenance of long-term tolerance. Importantly, the role of Foxp3(+) Treg and Tr1 cells is not redundant once they are simultaneously expanded/induced in the same host. Moreover, our data show that long-term tolerance induced by Foxp3(+) Treg-cell transfer is sustained by splenic Tr1 cells and functionally moves from the allograft to the spleen.
View details for DOI 10.1111/ajt.12333
View details for Web of Science ID 000322330000008
View details for PubMedID 23834659