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Author Notes:

Address Correspondence to: Allan D. Kirk, MD, PhD, 101 Woodruff Circle, 5105WMB, Atlanta, Georgia 30322 USA, Tel: 404.727.8380, Fax: 404-727-3660, ADKirk@emory.edu

Subject:

Research Funding:

ADK is supported by the National Institutes of Health (1U01AI079223-01A1), the Georgia Research Alliance, the McKelvey Foundation, and the Juvenile Diabetes Research Foundation.

MLF is supported by the National Institutes of Health (AI 079409).

Keywords:

  • memory T cell
  • heterologous immunity
  • homeostatic proliferation
  • tolerance
  • allograft

Memory T Cell-Specific Therapeutics in Organ Transplantation

Tools:

Journal Title:

Current Opinion in Organ Transplantation

Volume:

Volume 14, Number 6

Publisher:

, Pages 643-649

Type of Work:

Article | Post-print: After Peer Review

Abstract:

Purpose of the Review This review details the role of memory T cells in physiologic and allospecific immunity, and summarizes the effects of immunosuppressive agents used to manipulate their function in the context of organ transplantation. Recent Findings Memory T cells are lymphocytes with characteristics that are thought to promote anamnestic immune responses. They have a unique capacity to generate rapid effector functions upon secondary exposure to a pathogen, and this is achieved through truncated requirements for antigen presentation, reduced activation thresholds, and enhanced trafficking and adhesion mechanisms. In general, these same mechanisms also appear to evoke improved efficiency in mediating allograft rejection. The phenotype of these cells has been increasingly well defined and associated with a characteristic pattern of susceptibility to immunosuppressive agents. This knowledge is now being exploited in the development of immune therapeutic regimens to selectively mollify T memory cell effects. Summary A specific targeting of memory T cells has potential to prevent allograft rejection in a more precise manner that current means of immunosuppression. However, these benefits will be balanced by the reciprocal risk of susceptibility to recurrent infection.

Copyright information:

© Lippincott Williams & Wilkins. Unauthorized reproduction of this article is prohibited.

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