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Modulation of Memory T Cells to Control Acquired Bone Marrow Failure

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Technical Report,01 Sep 2011,30 Sep 2015

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Temple University Philadelphia, United States

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Acquired aplastic anemia AA is a fatal disorder characterized by immune-mediated destruction of hematopoietic stem and progenitorcells.1 Immunosuppressive therapy and allogeneic BMT have significantly improved the survival of severe AA.However, relapse still occurs in approximately 35 of AA patients when immunosuppressive therapy iswithdrawn.2,3 Furthermore, GVHD remains a major barrier to the success of allogeneic BMT.4,5 Memory T cells maypresent a significant barrier to the success of controlling various inflammatory conditions. Memory T cells, derivedfrom proliferating T cells during primary immune response,6-13 can undergo self-renewal to survive throughout thelifetime of an individual and continually generate differentiated effector T cells.9-11,14-18 Compared to nave T cells,memory T cells respond more rapidly to T cell receptor TCR activation, require lower concentrations of antigen andare less dependent on costimulatory signals such as CD28.6,7,9,11,15,19 This could explain that memory T cells canbe refractory to many of the tolerance-inducing strategies and immunosuppressive agents that are effective againstnave T cells.20,21 Notably, BM can function as a secondary lymphoid organ where memory T cells are maintained asresting cells undergoing homeostasis and can be reactivated to become effector T cells.22,23 These observationssuggest that memory T cells could be responsible for the relapse and treatment refractory of AA.

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