Research Papers:

CD200fc enhances anti-tumoral immune response and inhibits visceral metastasis of breast carcinoma

Nuray Erin _, Gamze Tanrıöver, Anna Curry, Muhlis Akman, Özlem Duymuş and Reg Gorczynski

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Oncotarget. 2018; 9:19147-19158. https://doi.org/10.18632/oncotarget.24931

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Nuray Erin1, Gamze Tanrıöver2, Anna Curry3, Muhlis Akman1, Özlem Duymuş1 and Reg Gorczynski3

1Department of Medical Pharmacology, Akdeniz University, School of Medicine, Antalya, Turkey

2Histology and Embryology, Akdeniz University, School of Medicine, Antalya, Turkey

3University Health Network, Toronto General Hospital, Toronto, Canada

Correspondence to:

Nuray Erin, email: [email protected]

Keywords: CD200fc; lung metastasis; liver metastasis; breast cancer

Received: August 21, 2017     Accepted: February 28, 2018     Published: April 10, 2018


CD200 is a widely expressed cell surface glycoprotein that inhibits excessive inflammation in autoimmunity, transplantation, and viral infections. We previously observed that visceral metastasis of highly aggressive and inflammatory 4THM breast carcinoma cells was markedly decreased in CD200 transgenic mice. The goal of this study was to determine whether exogenous exposure to CD200fc mimics the effects of endogenously over expressed CD200. Female BALB/c mice were injected with CD200fc two times a week for five times. Injection was started two days after orthotopic injection of 4THM cells. Tumor infiltrating Gr1+Cd11b+ cells were decreased while CD8+ cells were increased in CD200fc-treated animals. CD200fc injection significantly decreased lung and liver metastasis and the growth of primary tumors. CD200fc injection enhanced the tumor-induced IFN-g response while suppressing the IL-10 response. We observed excessive basal IL-6 secretion in MLC which was significantly decreased in CD200fc treated mice 12 days after injection of 4TM cells. These results are in accord with previous data from CD200 transgenic mice, and demonstrate for the first time that CD200 analogues might have therapeutic potential in the treatment of aggressive breast carcinoma which induces excessive systemic inflammation.

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