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HLA-B<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M3\"><mml:msup><mml:mrow\/><mml:mrow><mml:mo>\u2217<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:math>27 heavy chain (B27-HC) has an intrinsic propensity to fold slowly, leading to the accumulation of the misfolded B27-HC in the endoplasmic reticulum (ER) and formation of the HLA-B<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M4\"><mml:msup><mml:mrow\/><mml:mrow><mml:mo>\u2217<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:math>27 HC homodimer, (B27-HC)<jats:sub>2<\/jats:sub>, by a disulfide linkage at Cys-67. (B27-HC)<jats:sub>2<\/jats:sub>displayed on the cell surface can act as a ligand of the killer-cell Ig-like receptor (KIR3DL2). (B27-HC)<jats:sub>2<\/jats:sub>binds to KIR3DL2 of NK and Th17 cells and activates both cells, resulting in the activation of the IL-23\/IL-17 axis to launch the inflammatory reaction in AS patients. However, activation of the IL-23\/IL-17 axis originally derived from the HLA-B<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M5\"><mml:msup><mml:mrow\/><mml:mrow><mml:mo>\u2217<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:math>27 misfolding in the ER needs to be characterized. In this study, we delivered two HLA-B<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M6\"><mml:msup><mml:mrow\/><mml:mrow><mml:mo>\u2217<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:math>27-binding peptides, KRGILTLKY and SRYWAIRTR, into the ER by using a tat-derived peptide (GRKKRRQRRR)-His<jats:sub>6<\/jats:sub>-ubiquitin (THU) vehicle. Both peptides are derived from the human actin and nucleoprotein of influenza virus, respectively. Our results demonstrated that targeted delivery of both HLA-B<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M7\"><mml:msup><mml:mrow\/><mml:mrow><mml:mo>\u2217<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:math>27-binding peptides into the ER can promote the HLA-B<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M8\"><mml:msup><mml:mrow\/><mml:mrow><mml:mo>\u2217<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:math>27 folding, decrease the levels of (B27-HC)<jats:sub>2<\/jats:sub>, and suppress the activation of the IL-23\/IL-17 axis in response to lipopolysaccharide. Our findings can provide a new therapeutic strategy in AS.<\/jats:p>","DOI":"10.1155\/2017\/4016802","type":"journal-article","created":{"date-parts":[[2017,12,31]],"date-time":"2017-12-31T23:31:57Z","timestamp":1514763117000},"page":"1-10","source":"Crossref","is-referenced-by-count":6,"title":["Targeted Delivery of the HLA-B<mml:math xmlns:mml=\"http:\/\/www.w3.org\/1998\/Math\/MathML\" id=\"M1\"><mml:msup><mml:mrow\/><mml:mrow><mml:mo>\u2217<\/mml:mo><\/mml:mrow><\/mml:msup><\/mml:math>27-Binding Peptide into the Endoplasmic Reticulum Suppresses the IL-23\/IL-17 Axis of Immune Cells in Spondylarthritis"],"prefix":"10.1155","volume":"2017","author":[{"given":"Hui-Chun","family":"Yu","sequence":"first","affiliation":[{"name":"Department of Medical Research, Dalin Tzu Chi Hospital, Buddhist Tzu Chi Medical Foundation, Chiayi, Taiwan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kuang-Yung","family":"Huang","sequence":"additional","affiliation":[{"name":"Division of 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