Reconstitution dynamics of plasmacytoid and myeloid dendritic cell precursors after allogeneic myeloablative hematopoietic stem cell transplantation

Author:

Fagnoni Francesco F.1,Oliviero Barbara1,Giorgiani Giovanna1,De Stefano Piero1,Dehò Anna1,Zibera Carlo1,Gibelli Nadia1,Maccario Rita1,Da Prada GianAntonio1,Zecca Marco1,Locatelli Franco1

Affiliation:

1. From the Dipartimento di Oncologia, Fondazione S. Maugeri, Istituto di Ricovero e Cura a Carattere Scientifico (IRCCS) Clinica del Lavoro e della Riabilitazione, Istituto Scientifico di Pavia, and Unità di Ematologia ed Oncologia Pediatrica, IRCCS Policlinico S. Matteo, Pavia, Italy.

Abstract

Abstract Dendritic cells (DCs) are fundamental for immunity. We investigated reconstitution of plasmacytoid DC (PDC) and myeloid DC (My-DC) precursors in the first 2 months after allogeneic hematopoietic stem cell transplantation (Allo-HSCT). Circulating DCs were monitored from the earliest phase of hematopoietic reconstitution in 43 children given standard therapy to prevent graft-versus-host disease (GVHD) and either treated or untreated with granulocyte colony-stimulating factor (G-CSF) after HSCT. In patients without GVHD, both My-DCs and PDCs reached consistently high absolute values during the initial phase. Time of engraftment did not differ between My-DCs and PDCs, regardless of administration of G-CSF. Treatment with G-CSF (1) accelerated early recovery of My-DC absolute numbers; (2) was associated with lower numbers of both My-DCs and PDCs in the later phase; and (3) significantly reduced the proportion of interleukin-12 (IL-12)–secreting cells. In some patients who developed acute GVHD, we found high numbers of circulating DC precursors during the early phase of this complication. However, treatment with steroids invariably induced rapid decrease of PDCs. Altogether, these data provide an evaluation of DC release after Allo-HSCT, indicate that postgrafting administration of G-CSF impairs the appearance of IL-12–producing DCs, and suggest that DC homeostasis may be disrupted at onset of GVHD.

Publisher

American Society of Hematology

Subject

Cell Biology,Hematology,Immunology,Biochemistry

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