Highly up-regulated CXCR3 expression on eosinophils in mice infected with Schistosoma japonicum

被引:0
|
作者
He, L
Hu, CS
Cai, GB
Zhang, QP
Li, Q
Zhang, XL
Huang, BJ
Zhang, LJ
Liu, JY
Jiang, MS
Tan, JQ
机构
[1] Wuhan Univ, Coll Med, Dept Immunol, Wuhan 430071, Peoples R China
[2] Wuhan Univ, Coll Med, Dept Parasitol, Wuhan 430071, Peoples R China
[3] Anhui Med Univ, Coll Basic Med Sci, Dept Immunol, Hefei, Peoples R China
关键词
D O I
10.1046/j.1365-2567.2003.01771.x
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
CXCR3, predominately expressed on memory/activated T cells, is a receptor for both interferon-gamma inducible protein-10/CXC ligand 10 (CXCL10) and monokine induced by interferon-gamma/CXCL9. We reported here that CXCR3 was highly up-regulated on infiltrating eosinophils in Schistosoma japonicum egg-induced granuloma in the mouse liver. It was also highly and functionally up-regulated on peritoneal exudate eosinophils in mice infected with S. japonicum. The phenomena were demonstrated at protein and mRNA levels using immunohisto- and immunocytochemistry evaluation of biopsy, flow cytometry and real-time quantitative reverse transcriptase-polymerase chain reaction technique, and verified by Northern blotting and chemotaxis assay in vitro. We also found that CCR3 expression on the infiltrating and peritoneal exudate cells was significantly decreased, CXCR4 expression was unchanged during the 42-day period of infection. We screened mRNA expression levels of the all known chemokine receptors in purified peritoneal exudate eosinophils and liver granuloma dominated by eosinophils. CXCR3 was highly and functionally up-regulated on peritoneal exudate eosinophils in mice infected with S. japonicum, meanwhile CCR3 was significantly and functionally down-regulated in these cells. The findings could lead to a better understanding of the chemokine receptor expression pattern of eosinophils at inflamed tissue sites caused by parasites. These could be also crucial for establishing a therapeutic strategy for eosinophilic inflammation via intervention in chemokine actions.
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页码:107 / 117
页数:11
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