Related Experiment Video
Updated: May 19, 2026
Murine Model of CD40-activation of B cells
Published on: March 5, 2010
Soluble CD200 is critical to engraft chronic lymphocytic leukemia cells in immunocompromised mice
Karrie K Wong1, Fred Brenneman, Alden Chesney
1Institute of Medical Science, University of Toronto, Toronto, Ontario, Canada.
Insights
Soluble CD200 (sCD200) is elevated in chronic lymphocytic leukemia (CLL) patients and promotes CLL cell engraftment in mice. Targeting sCD200 shows promise as a new therapy for CLL.
Area of Science:
- Immunology
- Hematology
- Oncology
Background:
- CD200 is an immunoregulatory molecule overexpressed in chronic lymphocytic leukemia (CLL).
- A novel soluble form, sCD200, was identified in human plasma.
Purpose of the Study:
- To characterize sCD200 and investigate its role in CLL pathogenesis.
- To evaluate sCD200 as a prognostic marker and therapeutic target for CLL.
Main Methods:
- Quantified sCD200 levels in CLL patients and healthy controls.
- Utilized a humanized mouse model (NSG mice) to assess CLL cell engraftment.
- Administered anti-CD200 monoclonal antibody (mAb) and OKT3 mAb in vivo.
Main Results:
- sCD200 levels were significantly higher in CLL patients, correlating with disease stage.
- sCD200 enhanced CLL splenocyte engraftment in NSG mice.
- Depletion of sCD200 or treatment with anti-CD200 mAb inhibited CLL engraftment.
- Anti-CD200 mAb demonstrated efficacy comparable to rituximab in eliminating engrafted CLL cells.
Conclusions:
- sCD200 is a novel prognostic marker for CLL.
- sCD200 represents a potential therapeutic target for CLL treatment.
- The developed humanized mouse model is valuable for preclinical assessment of CLL therapies.
Abstract:
CD200 is a transmembrane molecule with an important immunoregulatory role that is overexpressed on most chronic lymphocytic leukemia (CLL) cells. In this study, we characterized a previously unknown soluble form of this molecule in human plasma termed sCD200. Levels of sCD200 were elevated in the plasma of patients with CLL as compared with healthy controls, and there was a significant correlation with CLL disease stage. Infusion of sCD200(hi) CLL plasma into severely immunocompromised NOD.SCIDγ(c)(null) (NSG) mice enhanced the engraftment of CLL splenocytes as compared with mice receiving sCD200(lo) normal plasma. CLL cells were detected in both the spleen and peritoneal cavity of animals for up to 75 days. Engraftment of CLL cells did not occur after infusion of CLL plasma depleted of sCD200 and was abolished in mice treated with anti-CD200 or OKT3 monoclonal antibody (mAb), suggesting a role for both sCD200 and T cells in CLL engraftment. Notably, anti-CD200 mAb was as effective as rituximab in eliminating engrafted CLL cells when administered 21 days after engraftment. Taken together, our findings point to sCD200 as a novel prognostic marker and therapeutic target for CLL. Furthermore, the humanized mouse model described here may prove valuable to preclinically assess new treatment regimens for CLL.
