M cells expressing the complement C5a receptor are efficient targets for mucosal vaccine delivery

2011 ◽  
Vol 41 (11) ◽  
pp. 3219-3229 ◽  
Author(s):  
Sae-Hae Kim ◽  
Dae-Im Jung ◽  
In-Young Yang ◽  
Ju Kim ◽  
Kyung-Yeol Lee ◽  
...  
2018 ◽  
Vol 09 (02) ◽  
Author(s):  
Beenish Israr ◽  
Jaehan Kim ◽  
Sidra Anam ◽  
Faisal Rasheed Anjum

PLoS ONE ◽  
2014 ◽  
Vol 9 (4) ◽  
pp. e95160 ◽  
Author(s):  
Hua Hua Tong ◽  
Garrett Lambert ◽  
Yong Xing Li ◽  
Joshua M. Thurman ◽  
Gregory L. Stahl ◽  
...  

2008 ◽  
Vol 52 (4-5) ◽  
pp. 846-856 ◽  
Author(s):  
Imre Farkas ◽  
Patricia Varju ◽  
Emese Szabo ◽  
Erik Hrabovszky ◽  
Noriko Okada ◽  
...  

2019 ◽  
Vol 4 (35) ◽  
pp. eaav5951 ◽  
Author(s):  
Yoshishige Miyabe ◽  
Chie Miyabe ◽  
Vinidhra Mani ◽  
Thorsten R. Mempel ◽  
Andrew D. Luster

Chemoattractant-induced arrest of circulating leukocytes and their subsequent diapedesis is a fundamental component of inflammation. However, how tissue-derived chemoattractants are transported into the blood vessel lumen to induce leukocyte entry into tissue is not well understood. Here, intravital microscopy in live mice has shown that the “atypical” complement C5a receptor 2 (C5aR2) and the atypical chemokine receptor 1 (ACKR1) expressed on endothelial cells were required for the transport of C5a and CXCR2 chemokine ligands, respectively, into the vessel lumen in a murine model of immune complex–induced arthritis. Transported C5a was required to initiate C5aR1-mediated neutrophil arrest, whereas transported chemokines were required to initiate CXCR2-dependent neutrophil transdendothelial migration. These findings provide new insights into how atypical chemoattractant receptors collaborate with “classical” signaling chemoattractant receptors to control distinct steps in the recruitment of neutrophils into tissue sites of inflammation.


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