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Updated: Jan 30, 2026

Construction of a Preclinical Multimodality Phantom Using Tissue-mimicking Materials for Quality Assurance in Tumor Size Measurement
Published on: July 29, 2013
The pro-tumor effect of CD200 expression is not mimicked by agonistic CD200R antibodies
Zofia Pilch1, Katarzyna Tonecka1, Marcin Skorzynski1
1Department of Immunology, Medical University of Warsaw, Warsaw, Poland.
Abstract:
Tumor-infiltrating immune cells can impact tumor growth and progression. The inhibitory CD200 receptor (CD200R) suppresses the activation of myeloid cells and lack of this pathway results in a reduction of tumor growth, conversely a tumorigenic effect of CD200R triggering was also described. Here we investigated the role of CD200R activation in syngeneic mouse tumor models. We showed that agonistic CD200R antibody reached tumors, but had no significant impact on tumor growth and minor effect on infiltration of immune myeloid cells. These effects were reproduced using two different anti-CD200R clones. In contrast, we showed that CD200-deficiency did decrease melanoma tumor burden. The presence of either endogenous or tumor-expressed CD200 restored the growth of metastatic melanoma foci. On the basis of these findings, we conclude that blockade of the endogenous ligand CD200 prevented the tumorigenic effect of CD200R-expressing myeloid cells in the tumor microenvironment, whereas agonistic anti-CD200R has no effect on tumor development.
Insights
Blocking the CD200 ligand, not activating its receptor (CD200R), reduced melanoma tumor growth. This highlights CD200 as a potential therapeutic target in cancer immunotherapy.
Area of Science:
- Immunology
- Oncology
- Cancer Research
Background:
- Tumor-infiltrating immune cells influence cancer progression.
- The CD200 receptor (CD200R) pathway, which inhibits myeloid cell activation, has complex roles in tumor growth.
- Previous studies show both reduced tumor growth and tumorigenic effects upon CD200R pathway modulation.
Purpose of the Study:
- To investigate the role of CD200 receptor (CD200R) activation in syngeneic mouse tumor models.
- To determine the impact of agonistic anti-CD200R antibodies and CD200 deficiency on tumor development.
Main Methods:
- Utilized syngeneic mouse models for melanoma.
- Administered agonistic anti-CD200R antibodies (two clones).
- Assessed tumor growth, burden, and immune cell infiltration in CD200-deficient mice and in the presence of CD200.
Main Results:
- Agonistic anti-CD200R antibodies reached tumors but did not significantly impact tumor growth or myeloid cell infiltration.
- CD200 deficiency led to decreased melanoma tumor burden.
- Restoration of CD200 (endogenous or tumor-expressed) re-established melanoma growth.
Conclusions:
- Blockade of the endogenous ligand CD200 inhibits tumor growth by preventing the tumorigenic effects of CD200R-expressing myeloid cells.
- Agonistic anti-CD200R therapy showed no significant effect on tumor development in these models.
- Targeting the CD200 ligand may be a more effective strategy than CD200R activation for cancer immunotherapy.
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