scholarly journals Early peripheral blood and T-cell chimerism dynamics after umbilical cord blood transplantation supported with haploidentical cells

2013 ◽  
Vol 49 (2) ◽  
pp. 212-218 ◽  
Author(s):  
M Kwon ◽  
C Martínez-Laperche ◽  
P Balsalobre ◽  
D Serrano ◽  
J Anguita ◽  
...  
Keyword(s):  
T Cell ◽  
Cord Blood ◽  
Umbilical Cord ◽  
Umbilical Cord Blood ◽  
Peripheral Blood ◽  
Cord Blood Transplantation ◽  
Umbilical Cord Blood Transplantation ◽  
Blood Transplantation

scholarly journals T-cell recovery in adults and children following umbilical cord blood transplantation

2001 ◽  
Vol 7 (8) ◽  
pp. 454-466 ◽  
Author(s):  
Andreas K. Klein ◽  
Dhavalkumar D. Patel ◽  
Maria E. Gooding ◽  
Gregory D. Sempowski ◽  
Benny J. Chen ◽  
...  
Keyword(s):  
T Cell ◽  
Cord Blood ◽  
Umbilical Cord ◽  
Umbilical Cord Blood ◽  
Cord Blood Transplantation ◽  
Umbilical Cord Blood Transplantation ◽  
Cell Recovery ◽  
Blood Transplantation ◽  
Adults And Children

scholarly journals Umbilical cord blood transplantation without in vivo T-cell depletion for children with MHC class II deficiency

2018 ◽  
Vol 141 (6) ◽  
pp. 2279-2282.e2 ◽  
Author(s):  
Reem Elfeky ◽  
Juliana M. Furtado-Silva ◽  
Robert Chiesa ◽  
Kanchan Rao ◽  
Giovanna Lucchini ◽  
...  
Keyword(s):  
T Cell ◽  
Cord Blood ◽  
Umbilical Cord ◽  
Mhc Class Ii ◽  
Umbilical Cord Blood ◽  
Cord Blood Transplantation ◽  
Umbilical Cord Blood Transplantation ◽  
Blood Transplantation ◽  
Mhc Class Ii Deficiency

A Single Center Experience with Allogeneic Sibling Umbilical-Cord-Blood Transplantation in Children with Malignant and Non-Malignant Disease.

Blood ◽  
2005 ◽  
Vol 106 (11) ◽  
pp. 2042-2042
Author(s):  
Yongping Song ◽  
Yanli Zhang ◽  
Baijun Fang ◽  
Xudong Wei ◽  
Lulu Lu ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cord Blood ◽  
Median Time ◽  
Umbilical Cord ◽  
Umbilical Cord Blood ◽  
Cd4 T Cells ◽  
Cord Blood Transplantation ◽  
Umbilical Cord Blood Transplantation ◽  
Blood Transplantation

Abstract To study the outcome of allogeneic sibling umbilical-cord-blood transplantation (CBT) in children in China, we studied the records of 38 recipients of cord blood from HLA-identical siblings from 1998 through 2004. The mean age at transplant was 10.3+/−5.5 years. Diseases of the patients were leukemia (28), neuroblastoma (3), severe aplastic anaemia (3) and inborn errors of metabolism (four). A volume of 76–208 ml of cord blood was collected from sibling infants soon after delivery. HLA antigens were identical in 32 and one to three antigens mismatched in six. The patients received busulphan and cyclophosphamide as conditioning, and antithymocyte globulin was given to prevent graft rejection. The median number of collected nucleated cells was 3.5 x 107/kg nucleated cells (range, 2.0 to 10.2). T-cell reconstitution was evaluated by using combined approaches of phenotyping analysis of lymphocytes and assessment of ex vivo thymic function by measuring T-cell receptor (TCR) rearrangement excision circles (TRECs). The overall survival is 89% at the median observation time of 72 months. The median time for neutrophil engraftment (absolute neutrophil count >500/mm3) was 16 days (range, 10 to 41days). The median time to become transfusion independent after CBT was 27 days for platelets (range, 15 to 54) and was 28 days for packed red blood cells (range, 19 to 128). Acute GVHD (aGVHD)was observed in 20/38 patients and involved only skin in 16 patients, skin and liver or gut in 2 patients and all 3 organs in another 2 patients. Seventeen of 20 patients had grade 1 to 2 aGVHD toxicity, whereas 3 patients experienced grade 3 to 4 aGVHD. Chronic GVHD (cGVHD) developed in 12 patients. Acute transplant related mortality was 5.5%. Cause of death was persisting non-engraftment till day +100 after transplant. Late mortality occurred in 2 patients: one cGVHD associated haemorrhage 22 months after CBT and one cGVHD associated septicaemia 4 years after CBT. Immunologic reconstitution demonstrated that CBT resulted in consistent and stable T-, B- and natural killer (NK) cell development. The kinetics of development was such that T-cell development occurred between 65 to 180 days. Initial T-cell engraftment consisted predominantly of CD45RO+, CD3+, and CD4+ T cells, and at 12 to 24 months changed to CD45RA+, CD3+, and CD4+ T cells, indicating de novo maturation of T cells. During the first 5 months after transplantation, TCR repertoires were highly abnormal and TREC values low. However, in a longer follow-up (one years or more after transplantation) TREC values and TCR diversity increased and became normal. This data confirms that CBT still should be the first treatment choice if an HLA-identical sibling is available.

HHV6-Associated Limbic Encephalitis after Reduced-Intensity Umbilical Cord Blood Transplantation.

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 2208-2208
Author(s):  
Kazuya Ishiwata ◽  
Hisashi Yamamoto ◽  
Shinsuke Takagi ◽  
Masanori Tsuji ◽  
Daisuke Kato ◽  
...  
Keyword(s):  
Cord Blood ◽  
Umbilical Cord ◽  
Umbilical Cord Blood ◽  
Peripheral Blood ◽  
Limbic Encephalitis ◽  
Cord Blood Transplantation ◽  
High Signal ◽  
Umbilical Cord Blood Transplantation ◽  
Blood Transplantation ◽  
Reduced Intensity

Abstract Background: HHV6 reactivation has been increasingly recognized in allogeneic haematopoietic stem cell transplant recipients, particularly in umbilical cord blood transplantation. In adult recipients, HHV6 has been associated with limbic encephalitis (HHV6-LE), which causes anterograde amnesia and epilepsy. The CNS disorder confined to the hippocampal regions; the presence of abnormal MRI signals involving the hippocampus, and detection of HHV6 DNA inCSF. However, the clinical features of the syndrome have not been well characterized. Methods: In this study we retrospectively reviewed the medical records of 139 umbilical cord blood transplantation recipients with reduced-intensity conditioning between January 2006 and December 2007 at Toranomon Hospital in Japan to determine the incidence of HHV6-LE among these patients. The diagnosis was based on the acute development of retrograde amnesia, confusion, coma and seizures accompanied by charascteristic MRI findings of abnormal high signal intensity on flair and T2 weighted images in the hippocampus and mesial temporal lobes, and the detection of HHV6 DNA in CSF. Eighty-six were received foscarnet before the onset of HHV6-LE as prophylaxis. All the patients who manifested suspicious symptoms of HHV6-LE were treated with foscarnet. Results: HHV6-LE was diagnosed in 11/139 for a cumulative incidence of 7.2%. The median age was 49 years (range 36–82), 3 were female. Diseases treated were AML/MDS (8), ALL (1), diffuse large B-cell lymphoma (1), and aplastic anemia (1). All 11 were conditioned with fludarabine-based reduced-intensity regimen, and tacrolimus alone (5) or tacrolimus+mycophenolate mofetil (6) were used as GVHD prophylaxis. Five of them had started foscarnet before the onset of HHV6-LE as a prophylaxis. Median symptom onset was on day +20 (range, 12–50). Initial symptoms included confusion in 9, retrograde amnesia in 8, and seizures in 5. MRI demonstrated hyppocampal and mesial temporal lobe FLAIR/T2 high signal intensity in 8/11. Initial CSF analysis demonstrated a median WBC count was 7 (range, 1–21)/μl, median protein was 49 (range, 44–337) mg/dl, median glucose was 107 (range, 62–269) mg/dl. No positive results of bacterial or viral cultures were observed in any of the patients. Median HHV6 DNA levels in the CSF was 20000 (range, 200–80000) copies/ml. Median HHV6 DNA levels in peripheral blood was 200 (range, 0–300000) copies/ml. Remarkably, 7 patients were negative for HHV6 in peripheral blood even within 6 days prior to the onset of CNS symptoms. All were treated with foscarnet at 50–100mg/kg of body weight, and clinical symptoms improved in 9 evaluable patients (2 were not evaluable due to severe pulmonary complications). The virus was cleared in the CSF successfully in 7 patients evaluated. Seven died with the median survival of 32 days (range, 7–346) from diagnosis of limbic encephalitis. HHV6-LE was not a direct cause of death in any of them (2 were from infection, 2 from IP, 2 from relapse, and 1 from MOF). Four were alive as of July 31, 2008, and what is of extreme interest is that all were those who received foscarnet as a prophylaxis. None of the factors analysed failed to reach statistical significance regarding the impact on the onset of HHV6-LE. Conclusions: High incidence of HHV6-LE as well as reactivation of the virus was observed in CB recipients. HHV6 DNA monitoring in peripheral blood may not be sufficient to predict the development of HHV6-LE. Although clinical manifestations were severe in some cases, foscarnet therapy was effective in all evaluable cases. Possible positive impact of prophylactic foscarnet therapy on better survival was suggested, which needs further evaluation by prospective study.

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