scholarly journals Infusion of donor-derived CD8+ memory T cells for relapse following allogeneic hematopoietic cell transplantation

2018 ◽  
Vol 2 (6) ◽  
pp. 681-690 ◽  
Author(s):  
Lori Muffly ◽  
Kevin Sheehan ◽  
Randall Armstrong ◽  
Kent Jensen ◽  
Keri Tate ◽  
...  
Keyword(s):  
T Cells ◽  
Cell Transplantation ◽  
Hematopoietic Cell Transplantation ◽  
Memory T Cells ◽  
Hematopoietic Cell ◽  
Allogeneic Hematopoietic Cell Transplantation ◽  
Allogeneic Hct ◽  
Key Points ◽  
Cd8 Memory T Cells

Key Points Phenotypic TM isolation from unmanipulated donor apheresis via CD45RA depletion followed by CD8+ enrichment is feasible. TM infusion for patients with relapse after allogeneic HCT was safe and resulted in minimal GVHD.

scholarly journals Erythropoietin therapy after allogeneic hematopoietic cell transplantation: a prospective, randomized trial

Blood ◽  
2014 ◽  
Vol 124 (1) ◽  
pp. 33-41 ◽  
Author(s):  
Aurélie Jaspers ◽  
Frédéric Baron ◽  
Évelyne Willems ◽  
Laurence Seidel ◽  
Kaoutar Hafraoui ◽  
...  
Keyword(s):  
Randomized Trial ◽  
Cell Transplantation ◽  
Hematopoietic Cell Transplantation ◽  
Hematopoietic Cell ◽  
Allogeneic Hematopoietic Cell Transplantation ◽  
Prospective Randomized Trial ◽  
Allogeneic Hct ◽  
Transfusion Requirements ◽  
Key Points

Key Points Erythropoietin therapy can be effective to hasten erythroid recovery and reduce transfusion requirements after allogeneic HCT.

scholarly journals Vancomycin use and cytomegalovirus reactivation after allogeneic hematopoietic cell transplantation

2020 ◽  
Vol 4 (12) ◽  
pp. 2640-2643 ◽  
Author(s):  
Shijia Zhang ◽  
Ryan Shanley ◽  
Daniel J. Weisdorf ◽  
Armin Rashidi
Keyword(s):  
Cell Transplantation ◽  
Hematopoietic Cell Transplantation ◽  
Hematopoietic Cell ◽  
Allogeneic Hematopoietic Cell Transplantation ◽  
Allogeneic Hct ◽  
Gram Positive Bacteria ◽  
Cytomegalovirus Reactivation ◽  
Increased Risk ◽  
Key Points ◽  
Cmv Reactivation

Key Points Vancomycin exposure in the pre-engraftment period was associated with an increased risk for CMV reactivation after allogeneic HCT. Some gram-positive bacteria may protect against CMV reactivation.

High dose valacyclovir for cytomegalovirus prophylaxis following allogeneic hematopoietic cell transplantation

2021 ◽  
pp. 107815522110604
Author(s):  
Kelly G Hawks ◽  
Amanda Fegley ◽  
Roy T Sabo ◽  
Catherine H Roberts ◽  
Amir A Toor
Keyword(s):  
Cell Transplantation ◽  
Hematopoietic Cell Transplantation ◽  
Hematopoietic Cell ◽  
Allogeneic Hematopoietic Cell Transplantation ◽  
High Dose ◽  
Cmv Infection ◽  
Allogeneic Hct ◽  
Clinically Significant ◽  
Cmv Disease ◽  
Cmv Prophylaxis

Introduction Cytomegalovirus (CMV) is one of the most common and clinically significant viral infections following allogeneic hematopoietic cell transplantation (HCT). Currently available options for CMV prophylaxis and treatment present challenges related to side effects and cost. Methods In this retrospective medical record review, the incidence of clinically significant CMV infection (CMV disease or reactivation requiring preemptive treatment) following allogeneic HCT was compared in patients receiving valacyclovir 1 g three times daily versus acyclovir 400 mg every 12 h for viral prophylaxis. Results Forty-five patients who received valacyclovir were matched based on propensity scoring to 35 patients who received acyclovir. All patients received reduced-intensity conditioning regimens containing anti-thymocyte globulin. Clinically significant CMV infection by day + 180 was lower in the valacyclovir group compared to the acyclovir group (18% vs. 57%, p = 0.0004). Patients receiving valacyclovir prophylaxis also had less severe infection evidenced by a reduction in CMV disease, lower peak CMV titers, delayed CMV reactivation, and less secondary neutropenia. Conclusion Prospective evaluation of valacyclovir 1 g three times daily for viral prophylaxis following allogeneic HCT is warranted. Due to valacyclovir's favorable toxicity profile and affordable cost, it has the potential to benefit patients on a broad scale as an option for CMV prophylaxis.

scholarly journals Donor-Derived CD4+ T Cells and Human Herpesvirus 6B Detection After Allogeneic Hematopoietic Cell Transplantation

2020 ◽  
Author(s):  
Derek J Hanson ◽  
Hu Xie ◽  
Danielle M Zerr ◽  
Wendy M Leisenring ◽  
Keith R Jerome ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Transplantation ◽  
Cd4 T Cells ◽  
Hematopoietic Cell Transplantation ◽  
Mononuclear Cells ◽  
Human Herpesvirus ◽  
Hematopoietic Cell ◽  
Allogeneic Hematopoietic Cell Transplantation ◽  
Peripheral Blood Mononuclear

Abstract We sought to determine whether donor-derived human herpesvirus (HHV) 6B–specific CD4+ T-cell abundance is correlated with HHV-6B detection after allogeneic hematopoietic cell transplantation. We identified 33 patients who received HLA-matched, non–T-cell–depleted, myeloablative allogeneic hematopoietic cell transplantation and underwent weekly plasma polymerase chain reaction testing for HHV-6B for 100 days thereafter. We tested donor peripheral blood mononuclear cells for HHV-6B–specific CD4+ T cells. Patients with HHV-6B detection above the median peak viral load (200 copies/mL) received approximately 10-fold fewer donor-derived total or HHV-6B–specific CD4+ T cells than those with peak HHV-6B detection at ≤200 copies/mL or with no HHV-6B detection. These data suggest the importance of donor-derived immunity for controlling HHV-6B reactivation.

scholarly journals Multiple donor-derived leukemias in a recipient of allogeneic hematopoietic cell transplantation for myeloid malignancy

2020 ◽  
Vol 4 (19) ◽  
pp. 4798-4801
Author(s):  
Ibrahim Aldoss ◽  
Joo Y. Song ◽  
Peter T. Curtin ◽  
Stephen J. Forman
Keyword(s):  
Transplant Recipient ◽  
Myelodysplastic Syndrome ◽  
Cell Transplantation ◽  
Malignant Transformation ◽  
Hematopoietic Cell Transplantation ◽  
Hematopoietic Cell ◽  
Allogeneic Hematopoietic Cell Transplantation ◽  
Myeloid Malignancy ◽  
Key Points

Key Points A patient with myelodysplastic syndrome was transplanted twice and developed clonally unrelated relapse each time in donor-derived cells. This case supports the concept that a leukemogenic marrow environment may predispose the transplant recipient to malignant transformation.

scholarly journals Nonpermissive HLA-DPB1 mismatch increases mortality after myeloablative unrelated allogeneic hematopoietic cell transplantation

Blood ◽  
2014 ◽  
Vol 124 (16) ◽  
pp. 2596-2606 ◽  
Author(s):  
Joseph Pidala ◽  
Stephanie J. Lee ◽  
Kwang Woo Ahn ◽  
Stephen Spellman ◽  
Hai-Lin Wang ◽  
...  
Keyword(s):  
High Resolution ◽  
Cell Transplantation ◽  
Hematopoietic Cell Transplantation ◽  
Hematopoietic Cell ◽  
Allogeneic Hematopoietic Cell Transplantation ◽  
Unrelated Donor ◽  
Key Points ◽  
Overall Mortality

Key Points High-resolution matching for HLA-A, -B, -C, and -DRB1 is required for optimal survival in myeloablative-unrelated donor transplantation. HLA-DPB1 nonpermissive mismatches should be avoided in otherwise matched transplants to minimize overall mortality.

scholarly journals Pretransplant CSF-1 therapy expands recipient macrophages and ameliorates GVHD after allogeneic hematopoietic cell transplantation

2011 ◽  
Vol 208 (5) ◽  
pp. 1069-1082 ◽  
Author(s):  
Daigo Hashimoto ◽  
Andrew Chow ◽  
Melanie Greter ◽  
Yvonne Saenger ◽  
Wing-Hong Kwan ◽  
...  
Keyword(s):  
T Cells ◽  
T Cell ◽  
Cell Transplantation ◽  
Cell Expansion ◽  
Acute Gvhd ◽  
Hematopoietic Cell Transplantation ◽  
Hematopoietic Cell ◽  
Allogeneic Hematopoietic Cell Transplantation ◽  
Host Macrophage

Acute graft-versus-host disease (GVHD) results from the attack of host tissues by donor allogeneic T cells and is the most serious limitation of allogeneic hematopoietic cell transplantation (allo-HCT). Host antigen-presenting cells are thought to control the priming of alloreactive T cells and the induction of acute GVHD after allo-HCT. However, whereas the role of host DC in GVHD has been established, the contribution of host macrophages to GVHD has not been clearly addressed. We show that, in contrast to DC, reducing of the host macrophage pool in recipient mice increased donor T cell expansion and aggravated GVHD mortality after allo-HCT. We also show that host macrophages that persist after allo-HCT engulf donor allogeneic T cells and inhibit their proliferation. Conversely, administration of the cytokine CSF-1 before transplant expanded the host macrophage pool, reduced donor T cell expansion, and improved GVHD morbidity and mortality after allo-HCT. This study establishes the unexpected key role of host macrophages in inhibiting GVHD and identifies CSF-1 as a potential prophylactic therapy to limit acute GVHD after allo-HCT in the clinic.

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