NK cells play an important role in hematopoietic stem cell transplantation (HCT) and in cross talk with dendritic cells (DCs) to induce primary T cell response against infection. Therefore, we hypothesized that blood DCs should augment NK cell function and reduce the risk of leukemia relapse after HCT. To test this hypothesis, we conducted laboratory and clinical studies in parallel. We found that although, phenotypically, NK cells could induce DC maturation and DCs could in turn increase activating marker expression on NK cells, paradoxically, both BDCA1(+) myeloid DCs and BDCA4(+) plasmacytoid DCs suppressed the function of NK cells. Patients who received an HLA-haploidentical graft containing a larger number of BDCA1(+) DCs or BDCA4(+) DCs had a higher risk of leukemia relapse and poorer survival. Further experiments indicated that the potent inhibition on NK cell cytokine production and cytotoxicity was mediated in part through the secretion of IL-10 by BDCA1(+) DCs and IL-6 by BDCA4(+) DCs. These results have significant implications for future HCT strategies.

Background: Cardiac and liver iron assessment using magnetic resonance imaging (MRI) is non-invasive and used as a preclinical “endpoint” in asymptomatic patients and for serial iron measurements in iron-overloaded patients. Purpose: To compare iron measurements between hepatic and myocardial T2* and T2 at 1.5T and 3T MRI in normal and iron-overloaded patients. Material and Methods: The T2 and T2* values from the regions of interest (ROIs) at mid-left ventricle and mid-hepatic slices were evaluated by 1.5T and 3T MRI scans for healthy and iron-overloaded patients. Results: For iron-overloaded patients, the myocardial T2 (1.5T) and myocardial T2 (3T) values were 60.3 ms (range = 56.2–64.8 ms) and 55 ms (range = 51.6–60.1 ms) (ρ = 0.3679) while the myocardial T2* (3T) 20.5 ms (range = 18.4–25.9 ms) was shorter than the myocardial T2* (1.5T) 35.9 ms (range = 31.4–39.5 ms) (ρ = 0.6454). The hepatic T2 at 1.5T and 3T were 19.1 ms (range = 14.8–27.9 ms) and 15.5 ms (14.6–20.4 ms) (ρ = 0.9444) and the hepatic T2* at 1.5T and 3T were 2.7 ms (range = 1.8–5.6 ms) and 1.8 ms (range = 1.1–2.9 ms) (ρ = 0.9826). The line of best fit exhibiting the linearity of the hepatic T2* (1.5T) and hepatic T2* (3T) had a slope of 2 and an intercept of –0.387 ms (R = 0.984). Conclusion: Our study found myocardial T2 (1.5T) nearly equal to T2 (3T) with myocardial T2* (3T) 1.75 shorter than myocardial T2* (1.5T). The relationship of hepatic T2* (1.5T) and hepatic T2* (3T) was linear with T2* (1.5T) approximately double to T2* (3T) in iron-overloaded patients. This linear relationship between hepatic T2* (1.5T) and hepatic T2 (3T) could be an alternative method for estimating liver iron concentration (LIC) from 3T.