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10.1111/cei.12647 http://scihub22266oqcxt.onion/10.1111/cei.12647 C4557376!4557376 !25907714     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25907714 &cmd=llinks): Failed to open stream: HTTP request failed! 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Targeted IgA Fc receptor I (Fc?RI) therapy in the early intervention and treatment of pristane-induced lupus nephritis in mice |pdf=|usr=}}{{25907714 }} gab.com Text Targeted IgA Fc receptor I (Fc RI) therapy in the early intervention and treatment of pristane-induced lupus nephritis in mice JO: Clin Exp Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25907714 #FOAvip The Fc receptor I for IgA (Fc?RI) down-regulates humoral immune responses and modulates the risk of autoimmunity. This study aimed to investigate whether Fc?RI targeting can affect progression of pristine-induced lupus nephritis. In the first experiment (early intervention), four groups of animals were evaluated: untreated Fc?RI/FcR? transgenic (Tg) mice and Tg mice administered control antibody (Ctr Fab), saline and anti-Fc?RI Fab [macrophage inflammatory protein (MIP)-8a], respectively, three times a week for 29 weeks, after being injected once intraperitoneally with 0ˇ5 ml pristane. In the second experiment, antibody injection started after the onset of nephritis and was carried out for 2 months, with similar groups as described above. MIP-8a improved proteinuria, decreased the amounts of glomerular injury markers, serum interleukin (IL)-6, IL-1 and monocyte chemoattractant protein (MCP)-1, and F4/80 macrophages in the interstitium and glomeruli, in both experiments. When MIP-8a was used as early intervention, a decrease in mouse serum anti-nuclear antibody (ANA) titres and reduced deposition of immunoglobulins in glomeruli were observed. This effect was associated with reduced serum titres of immunoglobulin (Ig)G2a but not IgG1, IgG2b and IgG3. Furthermore, pathological analysis showed lower glomerular activity index and less fibronectin in MIP-8a treated mice. This study suggests that Fc?RI targeting could halt disease progression and lupus activation by selective inhibition of cytokine production, leucocyte recruitment and renal inflammation. Our findings provide a basis for the use of Fc?RI as a molecular target for the treatment of lupus. Twit Text FOAVip Targeted IgA Fc receptor I (Fc RI) therapy in the early intervention and treatment of pristane-induced lupus nephritis in mice ????Clin Exp Immunol http://www.kidney.de/pget.php?&tw=1&pmid=25907714 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25907714 #FOAvip English Wikipedia <ref>{{Cite pmid|25907714 }}</ref> Targeted IgA Fc receptor I (Fc?RI) therapy in the early intervention and treatment of pristane-induced lupus nephritis in mice #MMPMID25907714 Liu C ; Kanamaru Y ; Watanabe T ; Tada N ; Horikoshi S ; Suzuki Y ; Liu Z ; Tomino Y Clin Exp Immunol 2015[Sep]; 181 (3 ): 407-16 PMID25907714 show ga The Fc receptor I for IgA (Fc?RI) down-regulates humoral immune responses and modulates the risk of autoimmunity. This study aimed to investigate whether Fc?RI targeting can affect progression of pristine-induced lupus nephritis. In the first experiment (early intervention), four groups of animals were evaluated: untreated Fc?RI/FcR? transgenic (Tg) mice and Tg mice administered control antibody (Ctr Fab), saline and anti-Fc?RI Fab [macrophage inflammatory protein (MIP)-8a], respectively, three times a week for 29 weeks, after being injected once intraperitoneally with 0ˇ5 ml pristane. In the second experiment, antibody injection started after the onset of nephritis and was carried out for 2 months, with similar groups as described above. MIP-8a improved proteinuria, decreased the amounts of glomerular injury markers, serum interleukin (IL)-6, IL-1 and monocyte chemoattractant protein (MCP)-1, and F4/80 macrophages in the interstitium and glomeruli, in both experiments. When MIP-8a was used as early intervention, a decrease in mouse serum anti-nuclear antibody (ANA) titres and reduced deposition of immunoglobulins in glomeruli were observed. This effect was associated with reduced serum titres of immunoglobulin (Ig)G2a but not IgG1, IgG2b and IgG3. Furthermore, pathological analysis showed lower glomerular activity index and less fibronectin in MIP-8a treated mice. This study suggests that Fc?RI targeting could halt disease progression and lupus activation by selective inhibition of cytokine production, leucocyte recruitment and renal inflammation. Our findings provide a basis for the use of Fc?RI as a molecular target for the treatment of lupus. |Animals [MESH] |Antibodies, Monoclonal/immunology/*pharmacology [MESH] |Antigens, CD/genetics/immunology [MESH] |Autoantibodies/blood/immunology [MESH] |Cytokines/blood/immunology [MESH] |Enzyme-Linked Immunosorbent Assay [MESH] |Humans [MESH] |Immunoglobulin G/blood/immunology [MESH] |Kidney/drug effects/pathology/ultrastructure [MESH] |Lupus Nephritis/chemically induced/immunology/*prevention & control [MESH] |Mice, Inbred C57BL [MESH] |Mice, Transgenic [MESH] |Microscopy, Electron [MESH] |Molecular Targeted Therapy/*methods [MESH] |Receptors, Fc/*antagonists & inhibitors/genetics/immunology [MESH] |Terpenes [MESH]Targeted IgA Fc receptor I (Fc?RI) therapy in the early intervention a(epmc).pdf DeepDyve Pubget Overpricing