Regulation of leukocyte migration across endothelial barriers by ECTO-5′-Nucleotidase-Generated adenosine

被引：21
|
作者：
Thompson, Linda F. [1 ]
Takedachi, Masahide [1 ]
Ebisuno, Yukihiko [1 ]
Tanaka, Toshiyuki [2 ]
Miyasaka, Masayuki [3 ]
Mills, Jeffery H. [4 ]
Bynoe, Margaret S. [4 ]
机构：
[1] Oklahoma Med Res Fdn, Oklahoma City, OK 73104 USA
[2] Hyogo Univ Hlth Sci, Kobe, Hyogo, Japan
[3] Osaka Univ, Grad Sch Med, Osaka, Japan
[4] Cornell Univ, Coll Vet Med, Ithaca, NY 14853 USA
来源：
NUCLEOSIDES NUCLEOTIDES & NUCLEIC ACIDS | 2008年 / 27卷 / 6-7期
关键词：
CD73; ecto-5 '-nucleotidase; leukocyte migration; experimental autoimmune encephalomyelitis;
D O I：
10.1080/15257770802145678
中图分类号：
Q5 [生物化学]; Q7 [分子生物学];
学科分类号：
071010 ; 081704 ;
摘要：
CD73-deficient mice are valuable for evaluating the ability of CD73-generated adenosine to modulate adenosine receptor-mediated responses. Here we report the role of CD73 in regulating lymphocyte migration across two distinct barriers. In the first case, CD73-generated adenosine restricts the migration of lymphocytes across high endothelial venules (HEV) into draining lymph nodes after an inflammatory stimulus, apparently by triggering A2B receptors on HEV. Secondly, CD73 promotes the migration of pathogenic T cells into the central nervous system during experimental autoimmune encephalomyelitis. Experiments are in progress to determine whether this effect is also adenosine receptor-mediated and to identify the relevant adenosine receptor.
引用
收藏
页码：755 / 760
页数：6
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