Peripheral blood progenitor cell product contains Th1-biased noninvariant CD1d-reactive natural killer T cells: Implications for posttransplant survival Article

cited authors

  • Shaulov, A; Yue, S; Wang, RJ; Joyce, RM; Balk, SP; Kim, HT; Avigan, DE; Uhl, L; Sackstein, R; Exley, MA

fiu authors

abstract

  • Objective: Bone marrow (BM) Th1 populations can contribute to graft-vs-leukemia responses. Granulocyte/granulocyte macrophage colony-stimulating factor (CSF)-mobilized peripheral blood progenitor cells (PBPC) have become widely accepted alternatives to BM transplantation. T cells coexpressing natural killer cell proteins (NKT) include a CD1d-reactive subset that influences immunity by rapidly producing large amounts of Th1 and/or Th2 cytokines dependent upon microenvironment and disease. There are two types of CD1d-reactive NKT. iNKT express a semi-invariant T-cell receptor-α. Other noninvariant CD1d-reactive NKT from BM and liver produce large amounts of interleukin-4 or interferon-γ, respectively, and within the intestine can be biased in either direction. Recent data suggests that NKT might contribute to clinical benefits of PBPC. Materials and Methods: To address these issues, we phenotypically and functionally studied PBPC NKT. Results: Similarly to BM, NKT-like cells were common in allogeneic and autologous PBPC, there were relatively few classical iNKT, but high CD1d-reactivity concentrated in NKT fractions. Significantly, PBPC CD1d-reactive cells were relatively Th1-biased and their presence was associated with better prognosis. Granulocyte CSF treatment of BM to yield PBPC in vivo as well as in vitro Th2-polarizes conventional T cells and iNKT. However, granulocyte CSF treatment of BM in vitro produced Th1-biased NKT, providing a mechanism for opposite polarization of NKT from BM vs PBPC. Conclusions: These results suggest distinct Th1 CD1d-reactive NKT cells could stimulate anti-tumor responses from those previously described, which can suppress graft-vs-host disease. © 2008 ISEH - Society for Hematology and Stem Cells.

publication date

  • April 1, 2008

Digital Object Identifier (DOI)

start page

  • 464

end page

  • 472

volume

  • 36

issue

  • 4