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• W2012205832 startingPage "105" @default.
• W2012205832 abstract "After an inflammatory stimulus, lymphocyte migration into draining lymph nodes increases dramatically to facilitate the encounter of naive T cells with Ag-loaded dendritic cells. In this study, we show that CD73 (ecto-5′-nucleotidase) plays an important role in regulating this process. CD73 produces adenosine from AMP and is expressed on high endothelial venules (HEV) and subsets of lymphocytes. <i>Cd73</i>^−/− mice have normal sized lymphoid organs in the steady state, but ∼1.5-fold larger draining lymph nodes and 2.5-fold increased rates of L-selectin-dependent lymphocyte migration from the blood through HEV compared with wild-type mice 24 h after LPS administration. Migration rates of <i>cd73</i>^+/+ and <i>cd73</i>^−/− lymphocytes into lymph nodes of wild-type mice are equal, suggesting that it is CD73 on HEV that regulates lymphocyte migration into draining lymph nodes. The A_2B receptor is a likely target of CD73-generated adenosine, because it is the only adenosine receptor expressed on the HEV-like cell line KOP2.16 and it is up-regulated by TNF-α. Furthermore, increased lymphocyte migration into draining lymph nodes of <i>cd73</i>^−/− mice is largely normalized by pretreatment with the selective A_2B receptor agonist BAY 60-6583. Adenosine receptor signaling to restrict lymphocyte migration across HEV may be an important mechanism to control the magnitude of an inflammatory response." @default.
• W2012205832 created "2016-06-24" @default.
• W2012205832 creator A5009203630 @default.
• W2012205832 creator A5019601541 @default.
• W2012205832 date "2007-05-14" @default.
• W2012205832 modified "2023-10-16" @default.
• W2012205832 title "Current treatment of hepatitis B" @default.
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