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10.4049/jimmunol.1302249 http://scihub22266oqcxt.onion/10.4049/jimmunol.1302249 C4065838!4065838!24850720     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24850720&cmd=llinks): Failed to open stream: HTTP request failed! 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The combined role of galactose-deficient IgA1and streptococcal IgA-binding M protein in inducing IL-6 and C3 secretion from human mesangial cells: implications for IgA nephropathy |pdf=|usr=}}{{24850720}} gab.com Text The combined role of galactose-deficient IgA1and streptococcal IgA-binding M protein in inducing IL-6 and C3 secretion from human mesangial cells: implications for IgA nephropathy JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24850720 #FOAvip IgA nephropathy is characterized by mesangial cell proliferation and extracellular matrix expansion associated with immune deposits consisting of galactose-deficient polymeric IgA1 and C3. We have previously shown that IgA-binding regions of streptococcal M proteins co-localize with IgA in mesangial immune deposits in patients with IgA nephropathy. In the current study, the IgA-binding M4 protein from group A streptococcus was found to bind to galactose-deficient polymeric IgA1 with higher affinity than to other forms of IgA1, as shown by surface plasmon resonance and solid-phase immunoassay. The M4 protein was demonstrated to bind to mesangial cells not via the IgA-binding region but rather via the C-terminal region, as demonstrated by flow cytometry. IgA1 enhanced binding of M4 to mesangial cells, but not vice versa. Co-stimulation of human mesangial cells with M4 and galactose-deficient polymeric IgA1 resulted in a significant increase in IL-6 secretion compared to each stimulant alone. Galactose-deficient polymeric IgA1 alone, but not M4, induced C3 secretion from the cells and co-stimulation enhanced this effect. In addition, co-stimulation enhanced mesangial cell proliferation compared to each stimulant alone. These results indicate that IgA-binding M4 protein binds preferentially to galactose-deficient polymeric IgA1 and that these proteins together induce excessive pro-inflammatory responses and proliferation of human mesangial cells. Thus, tissue deposition of streptococcal IgA-binding M proteins may contribute to the pathogenesis of IgA nephropathy. Twit Text FOAVip The combined role of galactose-deficient IgA1and streptococcal IgA-binding M protein in inducing IL-6 and C3 secretion from human mesangial cells: implications for IgA nephropathy ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=24850720 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24850720 #FOAvip English Wikipedia <ref>{{Cite pmid|24850720}}</ref> The combined role of galactose-deficient IgA1and streptococcal IgA-binding M protein in inducing IL-6 and C3 secretion from human mesangial cells: implications for IgA nephropathy #MMPMID24850720 Schmitt R; Ståhl Al; Olin AI; Kristoffersson AC; Rebetz J; Novak J; Lindahl G; Karpman D J Immunol 2014[Jul]; 193 (1): 317-26 PMID24850720show ga IgA nephropathy is characterized by mesangial cell proliferation and extracellular matrix expansion associated with immune deposits consisting of galactose-deficient polymeric IgA1 and C3. We have previously shown that IgA-binding regions of streptococcal M proteins co-localize with IgA in mesangial immune deposits in patients with IgA nephropathy. In the current study, the IgA-binding M4 protein from group A streptococcus was found to bind to galactose-deficient polymeric IgA1 with higher affinity than to other forms of IgA1, as shown by surface plasmon resonance and solid-phase immunoassay. The M4 protein was demonstrated to bind to mesangial cells not via the IgA-binding region but rather via the C-terminal region, as demonstrated by flow cytometry. IgA1 enhanced binding of M4 to mesangial cells, but not vice versa. Co-stimulation of human mesangial cells with M4 and galactose-deficient polymeric IgA1 resulted in a significant increase in IL-6 secretion compared to each stimulant alone. Galactose-deficient polymeric IgA1 alone, but not M4, induced C3 secretion from the cells and co-stimulation enhanced this effect. In addition, co-stimulation enhanced mesangial cell proliferation compared to each stimulant alone. These results indicate that IgA-binding M4 protein binds preferentially to galactose-deficient polymeric IgA1 and that these proteins together induce excessive pro-inflammatory responses and proliferation of human mesangial cells. Thus, tissue deposition of streptococcal IgA-binding M proteins may contribute to the pathogenesis of IgA nephropathy. äThe combined role of galactose-deficient IgA1and streptococcal IgA-bin(epmc).pdf DeepDyve Pubget Overpricing