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10.1172/jci.insight.93688 http://scihub22266oqcxt.onion/10.1172/jci.insight.93688 C5499374!5499374!28679953     free     free     free Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 229.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       JCI+Insight ä ; 2 (13): ä Nephropedia Template TP {{tp|p=28679953|t=ä. Anti-citrullinated protein antibodies cause arthritis by cross-reactivity to joint cartilage |pdf=|usr=}}{{28679953}} gab.com Text Anti-citrullinated protein antibodies cause arthritis by cross-reactivity to joint cartilage JO: JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28679953 #FOAvip Today, it is known that autoimmune diseases start a long time before clinical symptoms appear. Anti-citrullinated protein antibodies (ACPAs) appear many years before the clinical onset of rheumatoid arthritis (RA). However, it is still unclear if and how ACPAs are arthritogenic. To better understand the molecular basis of pathogenicity of ACPAs, we investigated autoantibodies reactive against the C1 epitope of collagen type II (CII) and its citrullinated variants. We found that these antibodies are commonly occurring in RA. A mAb (ACC1) against citrullinated C1 was found to cross-react with several noncitrullinated epitopes on native CII, causing proteoglycan depletion of cartilage and severe arthritis in mice. Structural studies by X-ray crystallography showed that such recognition is governed by a shared structural motif ?RG-TG? within all the epitopes, including electrostatic potential-controlled citrulline specificity. Overall, we have demonstrated a molecular mechanism that explains how ACPAs trigger arthritis. Twit Text FOAVip Anti-citrullinated protein antibodies cause arthritis by cross-reactivity to joint cartilage ????JCI Insight http://www.kidney.de/pget.php?&tw=1&pmid=28679953 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28679953 #FOAvip English Wikipedia <ref>{{Cite pmid|28679953}}</ref> Anti-citrullinated protein antibodies cause arthritis by cross-reactivity to joint cartilage #MMPMID28679953 Ge C; Tong D; Liang B; Lönnblom E; Schneider N; Hagert C; Viljanen J; Ayoglu B; Stawikowska R; Nilsson P; Fields GB; Skogh T; Kastbom A; Kihlberg J; Burkhardt H; Dobritzsch D; Holmdahl R JCI Insight ä[]; 2 (13): ä PMID28679953show ga Today, it is known that autoimmune diseases start a long time before clinical symptoms appear. Anti-citrullinated protein antibodies (ACPAs) appear many years before the clinical onset of rheumatoid arthritis (RA). However, it is still unclear if and how ACPAs are arthritogenic. To better understand the molecular basis of pathogenicity of ACPAs, we investigated autoantibodies reactive against the C1 epitope of collagen type II (CII) and its citrullinated variants. We found that these antibodies are commonly occurring in RA. A mAb (ACC1) against citrullinated C1 was found to cross-react with several noncitrullinated epitopes on native CII, causing proteoglycan depletion of cartilage and severe arthritis in mice. Structural studies by X-ray crystallography showed that such recognition is governed by a shared structural motif ?RG-TG? within all the epitopes, including electrostatic potential-controlled citrulline specificity. Overall, we have demonstrated a molecular mechanism that explains how ACPAs trigger arthritis. äAnti-citrullinated protein antibodies cause arthritis by cross-reactiv(epmc).pdf DeepDyve Pubget Overpricing