Flt-3L expansion of recipient CD8α+ dendritic cells deletes alloreactive donor T cells and represents an alternative to posttransplant Cyclophosphamide for the prevention of GVHD

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Markey, Kate A.;Kuns, Rachel D.;Browne, Daniel J.;Gartlan, Kate H.;Robb, Renee J.;Martins, J. Paulo;Henden, Andrea S.;Minnie, Simone A.;Cheong, Melody;Koyama, Motoko;Smyth, Mark J.;Steptoe, Raymond J.;Belz, Gabrielle T.;Brocker, Thomas;Degli-Esposti, Mariapia A.;Lane, Steven W.;Hill, Geoffrey R.
Abstract

Purpose: Allogeneic bone marrow transplantation (BMT) provides curative therapy for leukemia via immunologic graft-versus-leukemia (GVL) effects. In practice, this must be balanced against life threatening pathology induced by graft-versus-host disease (GVHD). Recipient dendritic cells (DC) are thought to be important in the induction of GVL and GVHD. Experimental Design: We have utilized preclinical models of allogeneic BMT to dissect the role and modulation of recipient DCs in controlling donor T-cell–mediated GVHD and GVL. Results: We demonstrate that recipient CD8α+ DCs promote activation-induced clonal deletion of allospecific donor T cells after BMT. We compared pretransplant fms-like tyrosine kinase-3 ligand (Flt-3L) treatment to the current clinical strategy of posttransplant cyclophosphamide (PT-Cy) therapy. Our results demonstrate superior protection from GVHD with the immunomodulatory Flt-3L approach, and similar attenuation of GVL responses with both strategies. Strikingly, Flt-3L treatment permitted maintenance of the donor polyclonal T-cell pool, where PT-Cy did not. Conclusions: These data highlight pre-transplant Flt-3L therapy as a potent new therapeutic strategy to delete alloreactive T cells and prevent GVHD, which appears particularly well suited to haploidentical BMT where the control of infection and the prevention of GVHD are paramount. Clin Cancer Res; 1–13. ©2018 AACR.

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Clinical Cancer Research

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24

ISBN/ISSN

1557-3265

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Issue

7

Pages Count

14

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Publisher

American Association for Cancer Research

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DOI

10.1158/1078-0432.CCR-17-2148