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Specifically differentiated T cell subset promotes tumor immunity over fatal immunity.

Authors
  • Ramadan, Abdulraouf1
  • Griesenauer, Brad1
  • Adom, Djamilatou1
  • Kapur, Reuben1
  • Hanenberg, Helmut1
  • Liu, Chen2
  • Kaplan, Mark H1
  • Paczesny, Sophie3
  • 1 Indiana University School of Medicine, Indianapolis, IN. , (India)
  • 2 Rutgers Robert Wood Johnson Medical School, New Brunswick, NJ.
  • 3 Indiana University School of Medicine, Indianapolis, IN [email protected] , (India)
Type
Published Article
Journal
Journal of Experimental Medicine
Publisher
The Rockefeller University Press
Publication Date
Dec 04, 2017
Volume
214
Issue
12
Pages
3577–3596
Identifiers
DOI: 10.1084/jem.20170041
PMID: 29038366
Source
Medline
License
Unknown

Abstract

Allogeneic immune cells, particularly T cells in donor grafts, recognize and eliminate leukemic cells via graft-versus-leukemia (GVL) reactivity, and transfer of these cells is often used for high-risk hematological malignancies, including acute myeloid leukemia. Unfortunately, these cells also attack host normal tissues through the often fatal graft-versus-host disease (GVHD). Full separation of GVL activity from GVHD has yet to be achieved. Here, we show that, in mice and humans, a population of interleukin-9 (IL-9)-producing T cells activated via the ST2-IL-33 pathway (T9IL-33 cells) increases GVL while decreasing GVHD through two opposing mechanisms: protection from fatal immunity by amphiregulin expression and augmentation of antileukemic activity compared with T9, T1, and unmanipulated T cells through CD8α expression. Thus, adoptive transfer of allogeneic T9IL-33 cells offers an attractive approach for separating GVL activity from GVHD.

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