4.5 Article

CD200R, a co-inhibitory receptor on immune cells, predicts the prognosis of human hepatocellular carcinoma

期刊

IMMUNOLOGY LETTERS
卷 178, 期 -, 页码 105-113

出版社

ELSEVIER
DOI: 10.1016/j.imlet.2016.08.009

关键词

Hepatocellular carcinoma; CD200 receptor; Co-inhibitory receptor; Prognosis; Immunotherapy

资金

  1. National Basic Research Program of China [2013CB944903]
  2. National Natural Science Foundation of China [81302599, 91442112, 31670908, 31571440, 81272327]

向作者/读者索取更多资源

The inhibitory CD200:CD200 receptor axis is essential in preventing inflammatory responses during early microbial infection. It was reported in several tumor models that CD200 expression is closely associated to tumor progression and the blockade of this pathway may restore anti-tumor responses. Our study for the first time investigates the role of CD200:CD200R axis in relation to tumor progression and prognosis of human hepatocellular carcinoma. CD200 and CD200R protein expressions were evaluated by immunostaining on liver tissue specimens and we found higher expressions of CD200 and CD200R in HCC patients comparing to healthy controls. CD200 expresses in peritumoral, peritumoral stroma and intratumoral regions of HCC while CD200R predominantly expresses in peritumoral stroma. Furthermore, protein intensity of CD200R is positively associated to the diameter of tumor and alpha-fetoprotein level, in addition, patients with higher pathological grade and absence of tumor capsule exhibit higher CD200R expression. CD200R predominantly expresses on infiltrating macrophages and may associate with liver injury. Moreover, both overall and recurrence-free survival rates are significantly lower in patients with high CD200R expression comparing to those with low CD200R expression. Our findings suggest a promising role of CD200R as a prognostic marker in predicting elevated recurrence and reduced survival, and a potential therapeutic target in treating hepatocellular carcinoma. (C) 2016 European Federation of Immunological Societies. Published by Elsevier B.V. All rights reserved.

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