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10.1073/pnas.1413915111

http://scihub22266oqcxt.onion/10.1073/pnas.1413915111
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C4273345!4273345!25475856
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suck abstract from ncbi


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pmid25475856      Proc+Natl+Acad+Sci+U+S+A 2014 ; 111 (50): 17971-6
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  • Fc?RIIb inhibits immune complex-induced VEGF-A production and intranodal lymphangiogenesis #MMPMID25475856
  • Clatworthy MR; Harford SK; Mathews RJ; Smith KGC
  • Proc Natl Acad Sci U S A 2014[Dec]; 111 (50): 17971-6 PMID25475856show ga
  • Antibody (IgG) plays an important role in defense against infection and in the pathogenesis of autoimmune diseases such as systemic lupus erythematosus (SLE). Low affinity-activating fragment crystallizable gamma receptors (Fc?Rs) that bind IgG immune complexes (ICs) mediate many effector functions of antibody and are controlled by an inhibitory receptor, Fc?RIIb. Here we show a previously unappreciated role for IC in driving an expansion of lymphatic conduits within lymph nodes. This was dependent on macrophage VEGF-A production and inhibited by Fc?RIIb. Lymphangiogenesis and VEGF-A were increased in the lymph nodes of mice with arthritis and SLE and in macrophages obtained from people with a SLE-associated, defunctioning polymorphism in FCGR2B. These findings have implications for the pathogenesis and treatment of autoimmune diseases.
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