Journal
NUCLEOSIDES NUCLEOTIDES & NUCLEIC ACIDS
Volume 27, Issue 6-7, Pages 755-760Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15257770802145678
Keywords
CD73; ecto-5 '-nucleotidase; leukocyte migration; experimental autoimmune encephalomyelitis
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Funding
- NIAID NIH HHS [K22 AI057854, AI57854, R01 AI018220, R01 AI018220-21, AI18220] Funding Source: Medline
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI018220, K22AI057854] Funding Source: NIH RePORTER
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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.
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