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Ectodomain shedding of CD200 from the B-CLL cell surface is regulated by ADAM28 expression

Tal Twito1, Zhiqi Chen, Ismat Khatri

  • 1Transplant Research Division, University Health Network, Toronto General Hospital, University of Toronto, Canada.

Leukemia Research
|May 7, 2013
PubMed

Insights

ADAM28 enzymes are involved in the shedding of CD200 (a protein overexpressed in chronic lymphocytic leukemia). This shedding releases soluble CD200 (sCD200), a marker of poor prognosis in CLL patients.

Area of Science:

  • Immunology
  • Biochemistry
  • Oncology

Background:

  • CD200, a membrane glycoprotein, is overexpressed in chronic lymphocytic leukemia (CLL).
  • Soluble CD200 (sCD200) in serum correlates with poor prognosis in CLL.
  • ADAM (a disintegrin and metalloproteinase) enzymes are known to mediate membrane protein shedding.

Purpose of the Study:

  • To investigate the role of ADAM28 in the shedding of CD200 in CLL.
  • To determine the correlation between ADAM28 expression and sCD200 levels in CLL patients.

Main Methods:

  • Analysis of ADAM28 mRNA expression in CLL samples.
  • Measurement of plasma sCD200 levels.
  • In vitro studies using siRNA to inhibit ADAM28 and gene transfection to overexpress ADAM28 in CLL cells.

Main Results:

  • ADAM28 mRNA expression in CLL was correlated with plasma sCD200 levels.
  • ADAM28 expression correlated with sCD200 release from cultured CLL cells.
  • siRNA-mediated knockdown of ADAM28 reduced sCD200 release.
  • Transfection of ADAM28 into CD200-expressing cells enhanced sCD200 release.

Conclusions:

  • ADAM28 plays a significant role in the shedding of CD200 from B-cell CLL cells.
  • ADAM28 may represent a therapeutic target for modulating sCD200 levels in CLL.

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