Ex vivo fucosylation of third-party human regulatory T cells enhances anti-graft-versus-host disease potency in vivo

Blood. 2015 Feb 26;125(9):1502-6. doi: 10.1182/blood-2014-10-603449. Epub 2014 Nov 26.

Abstract

Adoptive therapy with regulatory T cells (Tregs) to prevent graft-versus-host disease (GVHD) would benefit from a strategy to improve homing to the sites of inflammation. We hypothesized that adding fucose to human Tregs, forming the Sialyl Lewis X moiety on P-selectin glycoprotein ligand-1, would improve their trafficking pattern. The selectin pathway recruiter, α-1,3-fucosyltransferase-VI enzyme, significantly increased Treg surface fucosylation (66% vs 8%). In a xenogenic GVHD mouse model, fucosylated Tregs showed prolonged periods of in vivo persistence. When given at a lower dose compared with the untreated Tregs, the murine recipients of fucosylated Tregs maintained weight, had ameliorated clinical GVHD, and improved survival (70% vs 30%; P < .0001). These preclinical data indicate that fucosylated human Tregs is an effective strategy for prevention of GVHD and, as such, warrants consideration for future clinical trials.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Blotting, Western
  • Cells, Cultured
  • Disease Models, Animal*
  • E-Selectin / metabolism
  • Female
  • Fetal Blood / cytology
  • Fetal Blood / immunology
  • Fetal Blood / metabolism
  • Flow Cytometry
  • Fucose / metabolism*
  • Fucosyltransferases / metabolism
  • Graft vs Host Disease / immunology*
  • Graft vs Host Disease / mortality
  • Graft vs Host Disease / prevention & control*
  • Humans
  • Membrane Glycoproteins / metabolism
  • Mice
  • Mice, Inbred NOD
  • Mice, SCID
  • Oligosaccharides / metabolism
  • Sialyl Lewis X Antigen
  • T-Lymphocytes, Regulatory / immunology*

Substances

  • E-Selectin
  • Membrane Glycoproteins
  • Oligosaccharides
  • P-selectin ligand protein
  • Sialyl Lewis X Antigen
  • Fucose
  • Fucosyltransferases
  • galactoside 3-fucosyltransferase