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Gina... T cell research indicates that if affected cells are given new T cells that are not affected... One could reasonably theorize... the end of certain viruses.
Janie
The coordinated expression of chemokines and receptors may be important in the directed migration of alloreactive T cells during graft-vs-host disease (GVHD). Recent work demonstrated in a murine model that transfer of CCR5-deficient (CCR5(-/-)) donor cells to nonconditioned haploidentical recipients resulted in reduced donor cell infiltration in liver and lymphoid tissues compared with transfer of CCR5(+/+) cells. To investigate the function of CCR5 during GVHD in conditioned transplant recipients, we transferred CCR5(-/-) or wild-type C57BL/6 (B6) T cells to lethally irradiated B6D2 recipients. Unexpectedly, we found an earlier time to onset and a worsening of GVHD using CCR5(-/-) T cells, which was associated with significant increases in the accumulation of alloreactive CD4(+) and CD8(+) T cells in liver and lung. Conversely, the transfer of CCR5(-/-) donor cells to nonirradiated recipients led to reduced infiltration of target organs, confirming previous studies and demonstrating that the role of CCR5 on donor T cells is dependent on conditioning of recipients. Expression of proinflammatory chemokines in target tissues was dependent on conditioning of recipients, such that CXCL10 and CXCL11 were most highly expressed in tissues of irradiated recipients during the first week post-transplant. CCR5(-/-) T cells were shown to have enhanced migration to CXCL10, and blocking this ligand in vivo improved survival in irradiated recipients receiving CCR5(-/-) T cells. Our data indicate that the effects of inhibiting CCR5/ligand interaction on donor T cells during GVHD differ depending on conditioning of recipients, a finding with potentially important clinical significance.
Nonalloreactive donor T cells undergo homeostatic proliferation upon transfer to lethally irradiated allogeneic recipients. To better understand the preferential effect of IL-7 on the posttransplant reconstitution of memory/activated T cells, we first analyzed the phenotype and proliferation of the various populations of donor T cells after allogeneic BMT, including (a) alloreactive T cells, mature T cells contained in the allograft that recognize host allo-antigens and cause GVHD; (b) nonalloreactive T cells, mature T cells in the allograft that do not recognize alloantigens but have been suggested to contribute to T cell reconstitution, especially in older recipients with diminished thymic function (17); and (c) donor hematopoietic stem cell–derived T cells, newly derived T cells that originate from the transplanted donor hematopoietic stem cells and have been generated through thymic (and possibly also through extrathymic) differentiation.
To assess the proliferative activity and cell surface antigen expression patterns of alloreactive and nonalloreactive donor T cells after transplantation, we transferred CFSE-labeled purified splenic T cells from B6 (Ly5.1) donors into lethally irradiated syngeneic (B6) and allogeneic (C3FeB6F1) recipients and analyzed the number of cell divisions and cell surface antigen expression daily for 7 days (Figure 2a, 64 hours, and data not shown). When transferred into a lethally irradiated syngeneic recipient, B6 (Ly5.1) T cells undergo not more than three cell cycles in 64 hours, which is in agreement with the slow proliferation described previously for homeostatic proliferation of mature T cells in lymphopenic hosts
I also have The METHOD OF EXPANDING DOUBLE NEGATIVE T CELLS, if you would want that as well!!
noooooooooooooooo................don't be sorry.
I've stepped out of my realm of things easily understood, and it takes me a while to wrap my head around it.
Senario--non irradiated specimen as doner
non irradiated speciment as host
allogenic transferrance. But can't be bone marrow. Must be simple tissue, blood plasma, or infusion.