Downregulation of CD36 results in reduced phagocytic ability of peritoneal macrophages of women with endometriosis

Pei Chin Chuang, Meng-Hsing Wu, Yutaka Shoji, Shaw-Jenq Tsai

研究成果: Article同行評審

60 引文 斯高帕斯(Scopus)

摘要

Endometriosis, defined as the growth of endometrial tissues outside of the uterine cavity, is a severe and complex disease affecting more than 10% of women. The aetiology of endometriosis is unclear but immune dysfunction might be an important factor for its development. The natural function of the immune system is to detect and destroy aberrant or abnormal cells. Failure of the immune system to eradicate these aberrant cells often results in disease pathogenesis. We report here that the phagocytic ability of macrophages is reduced in peritoneal macrophages isolated from women with endometriosis. In-depth investigation revealed that the level of CD36, a class B scavenger receptor, in peritoneal macrophages derived from women with endometriosis was lower than that in normal macrophages. Blockage of CD36 function by neutralized antibody or knocking down CD36 using siRNA impaired the phagocytic ability of normal macrophages. In contrast, forced expression of CD36 in macrophages isolated from women with endometriosis restored phagocytic ability. Taken together, we identified that the scavenger receptor CD36 is reduced in the peritoneal macrophages of women with endometriosis, which leads to a decrease of the phagocytic ability of macrophages. These findings revealed a potential mechanism of immune dysfunction during endometriosis development.

原文English
頁(從 - 到)232-241
頁數10
期刊Journal of Pathology
219
發行號2
DOIs
出版狀態Published - 2009 十月 1

All Science Journal Classification (ASJC) codes

  • 病理學與法醫學

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