Ensity conditioning [53]. This apparent discrepancy is probably 15900046 explained the fact than median ALC counts on day 0 were 110 (range, 10?440) cells/ml in current patient versus 0 (range, 0?22) cells/mL in the Dean et al. study, while median counts of CD3+ T cells were 0 (range, 0?900) cells/mL at the time of transplantation in Thiant et al. study. Il-15 levels were lower in nonmyeloablative patients conditioned with 2 Gy TBI than in those conditioned with 4 Gy TBI, purchase GSK0660 demonstrating that the release of IL-15 was proportional to the intensity of the conditioning regimen. As observed by Thiant et al. [46,52], there was a correlation between IL-7 and IL-15 levels on day 14 (but not on day 28) after transplantation, and an inverse correlation between IL-15 levels and NK cell counts. Other factors affecting IL-15 levels included high CRP levels. Several observations demonstrate that immune recovery depended mainly on HPE the first year after nonmyeloablative conditioning regimen in current patients. Firstly, there was a strong correlation between the number of infused T cells and high counts of CD4+ and CD8+ T cells, as previously observed [43,54]. Secondly, thymic function was minimal during the first 100 days ?after allo-HSCT given that levels of naive CD4+ T cells did notsignificantly increase the first 100 days after transplantation ?despite that some naive T cells can undergo HPE and keep their ?naive phenotype. Third, there was a correlation between high donor age and low counts of CD3+ T cells (P = 0.04), CD4+ T cells ?(P = 0.05), and naive CD4+ T cells (P = 0.021), as previously observed in patients given grafts after nonmyeloablative conditioning [55]. Despite that, we failed to find any significant association between IL-7 and/or IL-15 levels early after transplantation and increment of T cell subset counts from days 14?8 to day 80?00, even after adjusting for potentially confounding cofactors. A number of previous studies have demonstrated that high levels of IL-7 [46,52,53] and/or IL-15 [46,52] early after transplantation correlated with subsequent occurrence of grade II V acute GVHD, while others study failed to find such an association [51,56]. The largest study including data from 153 consecutive allogeneic transplant recipients given grafts after highdose conditioning and ATG observed no correlation between IL-7 levels early after transplantation and acute GVHD, while, interestingly, there was an inverse correlation between IL-15 levels early after transplantation and grade II V acute GVHD [57]. Further, a recent study demonstrated that administration of IL-7 after allogeneic T cell-depleted transplantation in humans did not increase acute GVHD [58]. In the current study, we did not observe any association between levels of IL-7 or IL-15 early after allo-HSCT and grade II V acute GVHD. The same was true after adjusting the analyses for potentially confounding cofactors. Differences in postgrafting immunosuppression might be the cause for these apparent discrepancies between studies. As example, it has been shown that tacrolimus (given in patients included in the current study) decreased T cell proliferation induced by IL-7 [59], and tacrolimus levels were kept high in our patients the first weeks after transplantation (median 18.6, 16.4, 14.9 and 14.3 mg/L on days 0, 7, 14 and 21 after transplantation, respectively) probably explaining the low relatively 1407003 incidence of acute GVHD observed [60]. In Gepotidacin site summary, these data suggest that IL-.Ensity conditioning [53]. This apparent discrepancy is probably 15900046 explained the fact than median ALC counts on day 0 were 110 (range, 10?440) cells/ml in current patient versus 0 (range, 0?22) cells/mL in the Dean et al. study, while median counts of CD3+ T cells were 0 (range, 0?900) cells/mL at the time of transplantation in Thiant et al. study. Il-15 levels were lower in nonmyeloablative patients conditioned with 2 Gy TBI than in those conditioned with 4 Gy TBI, demonstrating that the release of IL-15 was proportional to the intensity of the conditioning regimen. As observed by Thiant et al. [46,52], there was a correlation between IL-7 and IL-15 levels on day 14 (but not on day 28) after transplantation, and an inverse correlation between IL-15 levels and NK cell counts. Other factors affecting IL-15 levels included high CRP levels. Several observations demonstrate that immune recovery depended mainly on HPE the first year after nonmyeloablative conditioning regimen in current patients. Firstly, there was a strong correlation between the number of infused T cells and high counts of CD4+ and CD8+ T cells, as previously observed [43,54]. Secondly, thymic function was minimal during the first 100 days ?after allo-HSCT given that levels of naive CD4+ T cells did notsignificantly increase the first 100 days after transplantation ?despite that some naive T cells can undergo HPE and keep their ?naive phenotype. Third, there was a correlation between high donor age and low counts of CD3+ T cells (P = 0.04), CD4+ T cells ?(P = 0.05), and naive CD4+ T cells (P = 0.021), as previously observed in patients given grafts after nonmyeloablative conditioning [55]. Despite that, we failed to find any significant association between IL-7 and/or IL-15 levels early after transplantation and increment of T cell subset counts from days 14?8 to day 80?00, even after adjusting for potentially confounding cofactors. A number of previous studies have demonstrated that high levels of IL-7 [46,52,53] and/or IL-15 [46,52] early after transplantation correlated with subsequent occurrence of grade II V acute GVHD, while others study failed to find such an association [51,56]. The largest study including data from 153 consecutive allogeneic transplant recipients given grafts after highdose conditioning and ATG observed no correlation between IL-7 levels early after transplantation and acute GVHD, while, interestingly, there was an inverse correlation between IL-15 levels early after transplantation and grade II V acute GVHD [57]. Further, a recent study demonstrated that administration of IL-7 after allogeneic T cell-depleted transplantation in humans did not increase acute GVHD [58]. In the current study, we did not observe any association between levels of IL-7 or IL-15 early after allo-HSCT and grade II V acute GVHD. The same was true after adjusting the analyses for potentially confounding cofactors. Differences in postgrafting immunosuppression might be the cause for these apparent discrepancies between studies. As example, it has been shown that tacrolimus (given in patients included in the current study) decreased T cell proliferation induced by IL-7 [59], and tacrolimus levels were kept high in our patients the first weeks after transplantation (median 18.6, 16.4, 14.9 and 14.3 mg/L on days 0, 7, 14 and 21 after transplantation, respectively) probably explaining the low relatively 1407003 incidence of acute GVHD observed [60]. In summary, these data suggest that IL-.