Transfer of allogeneic CD62L- memory T cells without graft-versus-host disease.

@article{Chen2004TransferOA,
  title={Transfer of allogeneic CD62L- memory T cells without graft-versus-host disease.},
  author={Benny J Chen and Xiuyu Cui and Gregory D. Sempowski and Congxiao Liu and Nelson J. Chao},
  journal={Blood},
  year={2004},
  volume={103 4},
  pages={
          1534-41
        }
}
The major challenge in allogeneic hematopoietic cell transplantation is how to transfer allogeneic T-cell immunity without causing graft-versus-host disease (GVHD). Here we report a novel strategy to selectively prevent GVHD by depleting CD62L(+) T cells (naive and a subset of memory T cells). In unprimed mice, CD62L(-) T cells (a subset of memory T cells) failed to proliferate in response to alloantigens (which the mice have never previously encountered) and were unable to induce GVHD in… 
CD62L- memory T cells enhance T-cell regeneration after allogeneic stem cell transplantation by eliminating host resistance in mice.
TLDR
Alloreactive CD62L(-) T cells lost the reactivity over time and were eventually tolerant to alloantigens as a result of prolonged antigen exposure, suggesting a mechanism by which CD 62L(+) T cells were able to eliminate host resistance without causing GVHD.
Allospecific CD4(+) effector memory T cells do not induce graft-versus-host disease in mice.
Effector memory CD4+ T cells mediate graft-versus-leukemia without inducing graft-versus-host disease.
TLDR
These studies identify T(EMs) as a clinically applicable cell therapy for promoting GVL and immune reconstitution, particularly in MHC-mismatched haploidentical alloSCTs in which T cell-depleted allografts are commonly used to minimize GVHD.
Central Memory CD8+ T Cells Induce Graft-versus-Host Disease and Mediate Graft-versus-Leukemia1
TLDR
It is demonstrated that purified CD8+ TCM not specifically primed to alloantigens mediate GVHD in the MHC-mismatched C57BL/6 (B6)→BALB/c and the M HC-matched, multiple minor histocompatibility Ag-mISMatched C3H strain pairings, in contrast to what was previously thought.
Diseasefor the Persistence of Graft-versus-Host Alloreactive Memory T Cells Are Responsible
TLDR
Allogeneic memory T cells are generated in vivo during GVH reactions and are able to cause GVHD, resulting in persistent host tissue injury, indicating in vivo blockade of both alloreactive effector T cells.
Effector memory CD 4 T cells mediate graft-versus-leukemia without inducing graft-versus-host disease
TLDR
These studies identify TEMs as a clinically applicable cell therapy for promoting GVL and immune reconstitution, particularly in MHC-mismatched haploidentical alloSCTs in which T cell–depleted allografts are commonly used to minimize GVHD.
Host-reactive CD8+ memory stem cells in graft-versus-host disease
TLDR
In mouse models of human GVHD, a new subset of postmitotic CD44loCD62LhiCD8+ T cells are identified that generate and sustain all allogeneic T-cell subsets in GV HD reactions, including central memory, effector memory and effector CD8+T cells, while self-renewing.
A repertoire-independent and cell-intrinsic defect in murine GVHD induction by effector memory T cells.
Effector memory T cells (T(EM)) do not cause graft-versus-host disease (GVHD), though why this is has not been elucidated. To compare the fates of alloreactive naive (T(N)) or memory (T(M)) T cells,
Alloreactive Memory T Cells Are Responsible for the Persistence of Graft-versus-Host Disease1
TLDR
Allogeneic memory T cells are generated in vivo during GVH reactions and are able to cause GVHD, resulting in persistent host tissue injury, and in vivo blockade of both alloreactive effector and memory T cell-mediated host tissue Injury may prove to be valuable for GV HD prevention and treatment.
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