Therapeutic regulatory T-cell adoptive transfer ameliorates established murine chronic GVHD in a CXCR5-dependent manner

Blood. 2016 Aug 18;128(7):1013-7. doi: 10.1182/blood-2016-05-715896. Epub 2016 Jul 6.

Abstract

Chronic graft-versus-host disease (cGVHD) is a major complication of allogeneic hematopoietic stem cell transplantation. In cGVHD, alloreactive T cells and germinal center (GC) B cells often participate in GC reactions to produce pathogenic antibodies. Although regulatory T cells (Tregs) can inhibit GC reactions, Treg numbers are reduced in cGVHD, contributing to cGVHD pathogenesis. Here, we explored 2 means to increase Tregs in cGVHD: interleukin-2/monoclonal antibody (IL-2/mAb) complexes and donor Treg infusions. IL-2/mAb complexes given over 1 month were efficacious in expanding Tregs and treating established cGVHD in a multi-organ-system disease mouse model characterized by GC reactions, antibody deposition, and lung dysfunction. In an acute GVHD (aGVHD) model, IL-2/mAb complexes given for only 4 days resulted in rapid mortality, indicating IL-2/mAb complexes can drive conventional T-cell (Tcon)-mediated injury. In contrast, Treg infusions, which uniformly suppress aGVHD, increased Treg frequency and were effective in preventing the onset of, and treating, established cGVHD. Efficacy was dependent upon CXCR5-sufficient Tregs homing to, and inhibiting, GC reactions. These studies indicate that the infusion of Tregs, especially ones enriched for GC homing, may be desirable for cGVHD therapy. Although IL-2/mAb complexes can be efficacious in cGVHD, a cautious approach needs to be taken in settings in which aGVHD elements, and associated Tcon, are present.

MeSH terms

  • Acute Disease
  • Adoptive Transfer*
  • Animals
  • Antibodies, Monoclonal / therapeutic use
  • Chronic Disease
  • Disease Progression
  • Graft vs Host Disease / immunology*
  • Graft vs Host Disease / therapy*
  • Interleukin-2 / therapeutic use
  • Mice, Inbred C57BL
  • Receptors, CXCR5 / metabolism*
  • T-Lymphocytes, Regulatory / immunology*
  • Treatment Outcome

Substances

  • Antibodies, Monoclonal
  • CXCR5 protein, mouse
  • Interleukin-2
  • Receptors, CXCR5