Reduced NFAT1 protein expression in human umbilical cord blood T lymphocytes

Blood. 1999 Nov 1;94(9):3101-7.

Abstract

Umbilical cord blood (UCB) stem cells from related and unrelated allogeneic donors have emerged as novel treatment for patients with hematologic malignancies. The incidence and severity of acute graft-versus-host disease (GVHD) after UCB transplantation compares favorably with that observed in recipients of matched unrelated donor allogeneic grafts, but remains a major cause of morbidity and mortality. It has been shown that stimulated lymphocytes from UCB have reduced production of cytokines including interferon-gamma (IFN-gamma) and tumor necrosis factor-alpha (TNF-alpha), which play a role in GVHD pathophysiology. We investigated the molecular mechanisms underlying this reduced cytokine production by analyzing expression of nuclear factor of activated T cells-1 (NFAT1) in UCB T cells. We detected no constitutive expression of NFAT1 protein in unstimulated UCB T cells compared with adult T cells. Moreover, although NFAT1 expression in UCB T cells was upregulated after prolonged (40 hours) T-cell stimulation, it was only partially upregulated when compared with adult controls. Our observation of minimal NFAT1 expression after stimulation correlated with reduced cytoplasmic IFN-gamma and TNF-alpha production in UCB T cells studied simultaneously. Reduced NFAT1 expression may blunt amplification of donor UCB T-cell alloresponsiveness against recipient antigens, thereby potentially limiting GVHD incidence and severity after allogeneic UCB transplantation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • DNA-Binding Proteins / biosynthesis*
  • Fetal Blood*
  • Flow Cytometry
  • Humans
  • Lymphocyte Activation
  • NFATC Transcription Factors
  • Nuclear Proteins*
  • T-Lymphocytes / metabolism*
  • Transcription Factors / biosynthesis*
  • Up-Regulation

Substances

  • DNA-Binding Proteins
  • NFATC Transcription Factors
  • NFATC2 protein, human
  • Nuclear Proteins
  • Transcription Factors