Nsplantation 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 Peptide M immunosuppression might be the 22948146 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 incidence of acute GVHD observed [60]. In summary, these data suggest that IL-7 and IL-15 levels remain relatively low after DprE1-IN-2 site nonmyeloablative transplantation, and that IL-7 and IL-15 levels early after nonmyeloablative transplantation do not predict for acute GVHD.AcknowledgmentsThe authors are grateful to O. Dengis for excellent technical support.Author ContributionsTaking care of the patients: YB FB. Conceived and designed the experiments: MF YB FB. Performed the experiments: MdB MF MH MPM AG. Analyzed the data: MdB MF LS FB. Contributed reagents/ materials/analysis tools: MdB MF YB FB. Wrote the paper: MdB FB.
Microtia is reported to occur in 0.83 to 4.34 per 10,000 births, with higher incidences among males and those of Asian heritage [1]. Although the diagnosis of microtia encompasses a spectrum of phenotypes, ranging from “mild structural abnormalities to complete absence of the ear,” [1] even minor cases may incur psychological distress due to actual or perceived disfigurement and its effect on psychosocial functioning. Autologous reconstruction techniques, in which costal cartilage is harvested, sculpted to recreate the three-dimensional structureof the auricle, and implanted under the periauricular skin, 
are the current gold standard for reconstruction of microtia [2] and other auricular deformities. Among the benefits of this approach are long-term stability [2,3,4,5], a high degree of biocompatibility [6], the absence of antigenicity [3], and the potential for the graft to grow with the patient as he 1516647 matures [2,3,4]. Despite these advantages, the use of autologous costal cartilage incurs numerous drawbacks, including a limited donor site supply [4,5,7] and significant donor site morbidity [2,3,4,5,7,8,9]. Other notable drawbacks associated with this approach are the immenseTissue Engineering of Patient-Specific Auriclesdifficulty inherent to sculpting an anatomically correct patientspecific auricular facsimile [3,4,7] and the inability for costal cartilage to adequately approximate the complex biomechanical properties of native auricular elastic cartilage [3,9], all of which contribute to suboptimal aesthetic outcomes. For these reasons, a tissue engineering-driven solution has long been sought for auricular reconstruction. Such a strategy entails the fabrication of a scaffold (either naturally-derived, synthetic, or a combination of the two) recapitulating the three-dimensional structure of the native e.Nsplantation 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 22948146 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 incidence of acute GVHD observed [60]. In summary, these data suggest that IL-7 and IL-15 levels remain relatively low after nonmyeloablative transplantation, and that IL-7 and IL-15 levels early after nonmyeloablative transplantation do not predict for acute GVHD.AcknowledgmentsThe authors are grateful to O. Dengis for excellent technical support.Author ContributionsTaking care of the patients: YB FB. Conceived and designed the experiments: MF YB FB. Performed the experiments: MdB MF MH MPM AG. Analyzed the data: MdB MF LS FB. Contributed reagents/ materials/analysis tools: MdB MF YB FB. Wrote the paper: MdB FB.
Microtia is reported to occur in 0.83 to 4.34 per 10,000 births, with higher incidences among males and those of Asian heritage [1]. Although the diagnosis of microtia encompasses a spectrum of phenotypes, ranging from “mild structural abnormalities to complete absence of the ear,” [1] even minor cases may incur psychological distress due to actual or perceived disfigurement and its effect on psychosocial functioning. Autologous reconstruction techniques, in which costal cartilage is harvested, sculpted to recreate the three-dimensional structureof the auricle, and implanted under the periauricular skin, are the current gold standard for reconstruction of microtia [2] and other auricular deformities. Among the benefits of this approach are long-term stability [2,3,4,5], a high degree of biocompatibility [6], the absence of antigenicity [3], and the potential for the graft to grow with the patient as he 1516647 matures [2,3,4]. Despite these advantages, the use of autologous costal cartilage incurs numerous drawbacks, including a limited donor site supply [4,5,7] and significant donor site morbidity [2,3,4,5,7,8,9]. Other notable drawbacks associated with this approach are the immenseTissue Engineering of Patient-Specific Auriclesdifficulty inherent to sculpting an anatomically correct patientspecific auricular facsimile [3,4,7] and the inability for costal cartilage to adequately approximate the complex biomechanical properties of native auricular elastic cartilage [3,9], all of which contribute to suboptimal aesthetic outcomes. For these reasons, a tissue engineering-driven solution has long been sought for auricular reconstruction. Such a strategy entails the fabrication of a scaffold (either naturally-derived, synthetic, or a combination of the two) recapitulating the three-dimensional structure of the native e.
