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Co-expression of the toleragenic glycoprotein, CD200, with markers for cancer stem cells

Brian T Kawasaki1, Tashan Mistree, Elaine M Hurt

  • 1Cancer Stem Cell Section, Laboratory of Cancer Prevention, Center for Cancer Research, National Cancer Institute at Frederick, National Institutes of Health Frederick, 1050 Boyles Street, Building 560, Room 21-81, MD 21702, USA. kawasakib@mail.nih.gov

Biochemical and Biophysical Research Communications
|October 30, 2007
PubMed

Insights

Cancer stem cells may evade immune surveillance by co-expressing the glycoprotein CD200. This finding reveals a novel immune evasion mechanism in epithelial cancers, including prostate and breast cancer.

Area of Science:

  • Tumor immunology
  • Cancer stem cell biology
  • Immunosuppression

Background:

  • Immunological surveillance normally eliminates malignant cells.
  • Cancer cells develop evasion mechanisms to suppress or tolerate the immune system.
  • Cancer stem cells are implicated in tumor initiation and formation.

Purpose of the Study:

  • To investigate the role of cancer stem cells in immune evasion.
  • To determine if cancer stem cells express molecules involved in immune tolerance.
  • To identify novel mechanisms of tumor immune evasion.

Main Methods:

  • Co-expression analysis of CD200 and stem cell markers on various cancer types.
  • Immunohistochemical staining of tumor samples.
  • Flow cytometry analysis.

Main Results:

  • CD200 was found to be co-expressed with stem cell markers on prostate, breast, brain, and colon cancers.
  • This is the first report of an immunomodulatory molecule on epithelial cancer stem cells.
  • The findings suggest a mechanism for tumor immune evasion.

Conclusions:

  • Epithelial cancer stem cells may evade immune surveillance through CD200 expression.
  • CD200 on cancer stem cells represents a potential target for cancer immunotherapy.
  • This discovery opens new avenues for understanding and overcoming tumor-induced immunosuppression.

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