Impaired T- and NK-cell reconstitution after haploidentical HCT with posttransplant cyclophosphamide.


Journal

Blood advances
ISSN: 2473-9537
Titre abrégé: Blood Adv
Pays: United States
ID NLM: 101698425

Informations de publication

Date de publication:
26 01 2021
Historique:
received: 21 07 2020
accepted: 25 11 2020
entrez: 26 1 2021
pubmed: 27 1 2021
medline: 15 5 2021
Statut: ppublish

Résumé

Administration of posttransplant cyclophosphamide (PTCy) has significantly expanded the number of patients undergoing HLA-haploidentical hematopoietic cell transplantation (haplo-HCT). To examine immune reconstitution in these patients, we monitored T- and natural killer (NK)-cell recovery in 60 patients receiving bone marrow or peripheral blood stem cell (PBSC) grafts after haplo-HCT with PTCy and 35 patients receiving HLA-matched donor PBSC grafts with standard graft-versus-host disease (GVHD) prophylaxis. Compared with HLA-matched recipients, early T-cell recovery was delayed in haplo-HCT patients and skewed toward effector memory T cells with markedly reduced naive T cells. We found higher regulatory T (Treg)-cell/conventional T (Tcon)-cell ratios early after HCT and increased PD-1 expression on memory T cells. Within the haplo-HCT, patients who did not develop chronic GVHD (cGVHD) had higher PD-1 expression on central and effector memory CD4+ Treg cells at 1 month after transplant. These findings suggest an immunologic milieu that promotes immune tolerance in haplo-HCT patients. NK cells were decreased early after haplo-HCT with preferential expansion of immature CD56brightCD16- NK cells compared with matched donor transplants. One month after transplant, mass cytometry revealed enrichment of immature NK-cell metaclusters with high NKG2A, low CD57, and low killer-cell immunoglobulin-like receptor expression after haplo-HCT, which partially recovered 3 months post-HCT. At 2 months, immature NK cells from both groups were functionally impaired, but interleukin-15 priming corrected these defects in vitro. Increased immature/mature NK-cell ratios were associated with cytomegalovirus reactivation and increased incidence of cGVHD after haplo-HCT. These homeostatic imbalances in T- and NK-cell reconstitution after haplo-HCT reveal opportunities for early immune-based interventions to optimize clinical outcomes.

Identifiants

pubmed: 33496734
pii: S2473-9529(21)00054-9
doi: 10.1182/bloodadvances.2020003005
pmc: PMC7839379
doi:

Substances chimiques

Cyclophosphamide 8N3DW7272P

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

352-364

Subventions

Organisme : NCI NIH HHS
ID : P01 CA229092
Pays : United States

Informations de copyright

© 2021 by The American Society of Hematology.

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Auteurs

Benedetta Rambaldi (B)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.
Clinical and Experimental Sciences Department, Bone Marrow Transplant Unit, ASST Spedali Civili, University of Pavia, Brescia, Italy.

Haesook T Kim (HT)

Department of Data Sciences, Dana-Farber Cancer Institute, Harvard T.H. Chan School of Public Health, Boston, MA; and.

Carol Reynolds (C)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Sharmila Chamling Rai (S)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Yohei Arihara (Y)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Tomohiro Kubo (T)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Leutz Buon (L)

Department of BioInformatics and Data Science, Dana-Farber Cancer Institute, Harvard Medical School, Boston, MA.

Mahasweta Gooptu (M)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

John Koreth (J)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Corey Cutler (C)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Sarah Nikiforow (S)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Vincent T Ho (VT)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Edwin P Alyea (EP)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Joseph H Antin (JH)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Catherine J Wu (CJ)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Robert J Soiffer (RJ)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Jerome Ritz (J)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

Rizwan Romee (R)

Department of Medical Oncology, Dana-Farber Cancer Institute and Harvard Medical School, Boston, MA.

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