AI Article Synopsis

  • Bone marrow transplantation (BMT) can cure leukemia and lymphoma, but it causes a serious side effect known as graft-versus-host disease (GVHD) due to donor T cells.
  • Researchers are exploring ways to separate the anti-tumor benefits of donor T cells from the harmful effects of GVHD, focusing on the roles of regulatory NKT cells and donor Treg cells.
  • This review highlights how these immune cells prevent GVHD while still fighting tumors and discusses their interactions in both mouse models and human cases.

Article Abstract

Bone marrow transplantation (BMT) is a potentially curative treatment for patients with leukemia and lymphoma. Tumor eradication is promoted by the anti-tumor activity of donor T cells contained in the transplant; however, donor T cells also mediate the serious side effect of graft-versus-host disease (GVHD). Separation of GVHD from graft anti-tumor activity is an important goal of research in improving transplant outcome. One approach is to take advantage of the immunomodulatory activity of regulatory NKT cells and CD4(+)CD25(+) Treg of host and/or donor origin. Both host and donor NKT cells and donor Treg are able to prevent GVHD in murine models. In this review, we summarize the mechanisms of NKT cell- and Treg-mediated protection against GVHD in mice while maintaining graft anti-tumor activity. In addition, we also examine the interactions between NKT cells and Treg in the context of BMT, and integrate the data from murine experimental models with the observations made in humans.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2926162PMC
http://dx.doi.org/10.1002/eji.201040394DOI Listing

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