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10.1155/2015/369462 http://scihub22266oqcxt.onion/10.1155/2015/369462 C4629040!4629040 !26568960     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26568960 &cmd=llinks): Failed to open stream: HTTP request failed! 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Nonbilayer Phospholipid Arrangements Are Toll-Like Receptor-2/6 and TLR-4 Agonists and Trigger Inflammation in a Mouse Model Resembling Human Lupus |pdf=|usr=}}{{26568960 }} gab.com Text Nonbilayer Phospholipid Arrangements Are Toll-Like Receptor-2/6 and TLR-4 Agonists and Trigger Inflammation in a Mouse Model Resembling Human Lupus JO: J Immunol Res http://www.kidney.de/pget.php?&tw=1&pmid=26568960 #FOAvip Systemic lupus erythematosus is characterized by dysregulated activation of T and B cells and autoantibodies to nuclear antigens and, in some cases, lipid antigens. Liposomes with nonbilayer phospholipid arrangements induce a disease resembling human lupus in mice, including IgM and IgG antibodies against nonbilayer phospholipid arrangements. As the effect of these liposomes on the innate immune response is unknown and innate immune system activation is necessary for efficient antibody formation, we evaluated the effect of these liposomes on Toll-like receptor (TLR) signaling, cytokine production, proinflammatory gene expression, and T, NKT, dendritic, and B cells. Liposomes induce TLR-4- and, to a lesser extent, TLR-2/TLR-6-dependent signaling in TLR-expressing human embryonic kidney (HEK) cells and bone marrow-derived macrophages. Mice with the lupus-like disease had increased serum concentrations of proinflammatory cytokines, C3a and C5a; they also had more TLR-4-expressing splenocytes, a higher expression of genes associated with TRIF-dependent TLR-4-signaling and complement activation, and a lower expression of apoptosis-related genes, compared to healthy mice. The percentage of NKT and the percentage and activation of dendritic and B2 cells were also increased. Thus, TLR-4 and TLR-2/TLR-6 activation by nonbilayer phospholipid arrangements triggers an inflammatory response that could contribute to autoantibody production and the generation of a lupus-like disease in mice. Twit Text FOAVip Nonbilayer Phospholipid Arrangements Are Toll-Like Receptor-2/6 and TLR-4 Agonists and Trigger Inflammation in a Mouse Model Resembling Human Lupus ????J Immunol Res http://www.kidney.de/pget.php?&tw=1&pmid=26568960 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26568960 #FOAvip English Wikipedia <ref>{{Cite pmid|26568960 }}</ref> Nonbilayer Phospholipid Arrangements Are Toll-Like Receptor-2/6 and TLR-4 Agonists and Trigger Inflammation in a Mouse Model Resembling Human Lupus #MMPMID26568960 Wong-Baeza C ; Tescucano A ; Astudillo H ; Reséndiz A ; Landa C ; España L ; Serafín-López J ; Estrada-García I ; Estrada-Parra S ; Flores-Romo L ; Wong C ; Baeza I J Immunol Res 2015[]; 2015 (ä): 369462 PMID26568960 show ga Systemic lupus erythematosus is characterized by dysregulated activation of T and B cells and autoantibodies to nuclear antigens and, in some cases, lipid antigens. Liposomes with nonbilayer phospholipid arrangements induce a disease resembling human lupus in mice, including IgM and IgG antibodies against nonbilayer phospholipid arrangements. As the effect of these liposomes on the innate immune response is unknown and innate immune system activation is necessary for efficient antibody formation, we evaluated the effect of these liposomes on Toll-like receptor (TLR) signaling, cytokine production, proinflammatory gene expression, and T, NKT, dendritic, and B cells. Liposomes induce TLR-4- and, to a lesser extent, TLR-2/TLR-6-dependent signaling in TLR-expressing human embryonic kidney (HEK) cells and bone marrow-derived macrophages. Mice with the lupus-like disease had increased serum concentrations of proinflammatory cytokines, C3a and C5a; they also had more TLR-4-expressing splenocytes, a higher expression of genes associated with TRIF-dependent TLR-4-signaling and complement activation, and a lower expression of apoptosis-related genes, compared to healthy mice. The percentage of NKT and the percentage and activation of dendritic and B2 cells were also increased. Thus, TLR-4 and TLR-2/TLR-6 activation by nonbilayer phospholipid arrangements triggers an inflammatory response that could contribute to autoantibody production and the generation of a lupus-like disease in mice. |Animals [MESH] |Autoantibodies/biosynthesis/blood [MESH] |Chlorpromazine/pharmacology [MESH] |Cytokines/biosynthesis/blood [MESH] |Diglycerides/pharmacology [MESH] |Disease Models, Animal [MESH] |Female [MESH] |Flagellin/pharmacology [MESH] |Gene Expression Regulation [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Immunoglobulin G/biosynthesis/blood [MESH] |Immunoglobulin M/biosynthesis/blood [MESH] |Inflammation [MESH] |Lipopolysaccharides/pharmacology [MESH] |Liposomes/chemistry/*pharmacology [MESH] |Lupus Erythematosus, Systemic/chemically induced/genetics/*immunology/pathology [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Oligopeptides/pharmacology [MESH] |Phosphatidic Acids/chemistry/pharmacology [MESH] |Phosphatidylcholines/chemistry/pharmacology [MESH] |Phosphatidylserines/chemistry/pharmacology [MESH] |Toll-Like Receptor 2/agonists/genetics/*immunology [MESH] |Toll-Like Receptor 4/agonists/genetics/*immunology [MESH]Nonbilayer Phospholipid Arrangements Are Toll-Like Receptor-2/6 and TL(epmc).pdf DeepDyve Pubget Overpricing