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10.1038/ni.3035 http://scihub22266oqcxt.onion/10.1038/ni.3035 C4270928!4270928!25347465     free     free     free Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 231.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 265.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Nat+Immunol 2015 ; 16 (1): 75-84 Nephropedia Template TP {{tp|p=25347465|t=2015. The CLEC-2?podoplanin axis controls fibroblastic reticular cell contractility and lymph node microarchitecture |pdf=|usr=}}{{25347465}} gab.com Text The CLEC-2 podoplanin axis controls fibroblastic reticular cell contractility and lymph node microarchitecture JO: Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25347465 #FOAvip In lymph nodes, fibroblastic reticular cells (FRCs) form a collagen-based reticular network that supports migratory dendritic cells (DCs) and T cells and transports lymph. A hallmark of FRCs is their propensity to contract collagen, yet this function is poorly understood. Here, we demonstrate that podoplanin (PDPN) regulated actomyosin contractility in FRCs. Under resting conditions, when FRCs are unlikely to encounter mature DCs expressing the PDPN receptor, CLEC-2, PDPN endowed FRCs with contractile function and exerted tension within the reticulum. Upon inflammation, CLEC-2 on mature DCs potently attenuated PDPN-mediated contractility, resulting in FRC relaxation and reduced tissue stiffness. Disrupting PDPN function altered the homeostasis and spacing of FRCs and T cells, resulting in an expanded reticular network and enhanced immunity. Twit Text FOAVip The CLEC-2 podoplanin axis controls fibroblastic reticular cell contractility and lymph node microarchitecture ????Nat Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25347465 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25347465 #FOAvip English Wikipedia <ref>{{Cite pmid|25347465}}</ref> The CLEC-2?podoplanin axis controls fibroblastic reticular cell contractility and lymph node microarchitecture #MMPMID25347465 Astarita JL; Cremasco V; Fu J; Darnell MC; Peck JR; Nieves-Bonilla JM; Song K; Woodruff MC; Gogineni A; Onder L; Ludewig B; Weimer RM; Carroll MC; Mooney DJ; Xia L; Turley SJ Nat Immunol 2015[Jan]; 16 (1): 75-84 PMID25347465show ga In lymph nodes, fibroblastic reticular cells (FRCs) form a collagen-based reticular network that supports migratory dendritic cells (DCs) and T cells and transports lymph. A hallmark of FRCs is their propensity to contract collagen, yet this function is poorly understood. Here, we demonstrate that podoplanin (PDPN) regulated actomyosin contractility in FRCs. Under resting conditions, when FRCs are unlikely to encounter mature DCs expressing the PDPN receptor, CLEC-2, PDPN endowed FRCs with contractile function and exerted tension within the reticulum. Upon inflammation, CLEC-2 on mature DCs potently attenuated PDPN-mediated contractility, resulting in FRC relaxation and reduced tissue stiffness. Disrupting PDPN function altered the homeostasis and spacing of FRCs and T cells, resulting in an expanded reticular network and enhanced immunity. äThe CLEC-2?podoplanin axis controls fibroblastic reticular cell contra(epmc).pdf DeepDyve Pubget Overpricing