Insufficient ex vivo expansion of Valpha24(+) natural killer T cells in malignant lymphoma patients related to the suppressed expression of CD1d molecules on CD14(+) cells

Cytotherapy. 2008;10(5):497-506. doi: 10.1080/14653240802072747.

Abstract

Background: Valpha24(+) natural killer T (NKT) cell is a human counterpart of mice Valpha14(+) NKT cell that has a regulatory role for innate and acquired potential antitumor activity. The efficient expansion of NKT cells is an obstacle to the clinical application of Valpha24(+) NKT cells for immunotherapy.

Methods: We used mononuclear cells (MNC) obtained from the peripheral blood (PB) of normal healthy donor (HD) and malignant lymphoma (ML) patients before and after granulocyte colony-stimulating factor (G-CSF) treatment. MNC were cultured for 12 days with alpha-galactosylceramide (100 ng/mL) and interleukin-2 (IL-2; 100 U/mL).

Results: The fold expansion of Valpha24(+) NKT cells was higher in HD than in ML patients (208 versus 0.00), despite comparable numbers of Valpha24(+) NKT cells before culture. G-CSF administration enhanced the predominance of Valpha24(+) NKT cell fold expansion in HD compared with ML patients (1935 versus 1.95). After treatment with G-CSF, the expression of CD1d molecules was up-regulated in CD14(+) cells from HD but not ML patients. The fold expansion of Valpha24(+) NKT cells and CD1d expression on CD14(+) cells was strongly correlated in both HD and ML patients (r(2)=0.84). However, replacement of a patient's CD14(+) cells with HD cells did not increase the efficacy of Valpha24(+) NKT cell expansion.

Discussion: G-CSF-mobilized PB from ML patients has inhibitory characteristics for Valpha24(+) NKT cell expansion as a result of both monocytes and Valpha24(+) NKT cells. Multiple procedures would be needed for the expansion of patients' Valpha24(+) NKT cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Antigens, CD1 / genetics*
  • Antigens, CD1 / immunology
  • Antigens, CD1 / metabolism
  • Cell Proliferation
  • Cells, Cultured
  • Female
  • Galactosylceramides / pharmacology
  • Gene Expression Regulation, Neoplastic
  • Granulocyte Colony-Stimulating Factor / administration & dosage
  • Granulocyte Colony-Stimulating Factor / immunology
  • Humans
  • Immunity, Innate
  • Immunophenotyping
  • Immunotherapy, Adoptive*
  • Injections, Subcutaneous
  • Interleukin-2 / pharmacology
  • Killer Cells, Natural / immunology
  • Killer Cells, Natural / transplantation*
  • Leukocytes, Mononuclear / metabolism
  • Leukocytes, Mononuclear / pathology
  • Leukocytes, Mononuclear / transplantation
  • Lipopolysaccharide Receptors / biosynthesis
  • Lipopolysaccharide Receptors / genetics
  • Lipopolysaccharide Receptors / immunology
  • Lymphoma / immunology
  • Lymphoma / pathology
  • Lymphoma / therapy*
  • Male
  • Receptors, Antigen, T-Cell / biosynthesis
  • Receptors, Antigen, T-Cell / genetics
  • Receptors, Antigen, T-Cell / immunology
  • Recombinant Proteins / administration & dosage
  • Recombinant Proteins / immunology
  • Tumor Escape / genetics
  • Tumor Escape / immunology

Substances

  • Antigens, CD1
  • CD1b antigen
  • Galactosylceramides
  • Interleukin-2
  • Lipopolysaccharide Receptors
  • Receptors, Antigen, T-Cell
  • Recombinant Proteins
  • Valpha24 protein, human
  • alpha-galactosylceramide
  • Granulocyte Colony-Stimulating Factor