Abstract
Abstract Introduction: CD200 imparts an immunoregulatory signal through its receptor - CD200R1, leading to the suppression of tumor specific immunity. The mechanism of CD200:CD200R1 signaling pathway is still uncertain. The aim of this study was to investigate the expression pattern and localization of CD200 and its receptor CD200R1 in normal mucosa and rectal cancer patients. Material and Methods: The immunohistochemical expressions and localizations of CD200 and CD200R1 were examined in 140 rectal cancer patients. Seventy nine of 140 underwent the preoperative radiotherapy treatment and the others were untreated prior to the surgery. In addition, 121 matched normal rectal mucosa samples from the same patients were evaluated. Results: CD200 was expressed in normal mucosal epithelium and rectal cancer. Expression of CD200R1 was seen in normal mucosal epithelium and stromal cells of tumor samples. We found significant up-regulation of CD200 in rectal cancer tissues compared to the normal mucosa (P = 0.001). Interestingly, CD200R1 was overexpressed in stromal cells of rectal cancer patients presenting metastases compared to patients without metastases (P = 0.002). However, there is no difference in the expression levels between stromal cells and tumor cells. More than that, the up-regulation of CD2OO in tumor cells and CD200R1 overexpression in stromal cells was observed in 87 % of metastatic rectal cancer patients. These high expression levels of tumoral CD200 and stromal CD200R1 were significantly correlated with lymph node metastasis. Conclusions: Interaction of CD200 and CD200R1 and their expression profile might be useful to follow-up disease progression in terms of carcinogenesis and metastasis. Citation Format: Atil Bisgin, Wen Jian Meng, Gunnar Adell, Xiao Feng Sun. Interaction of CD200 overexpression on tumor cells with CD200R1 overexpression on stromal cells: An escape from the host immune response in rectal cancer patients. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 4001. doi:10.1158/1538-7445.AM2014-4001
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