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Targeting of Immune Cells by Dual TLR2/7 Ligands Suppresses Features of Allergic Th2 Immune Responses in Mice
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نویسنده
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laiño j. ,wangorsch a. ,blanco f. ,wolfheimer s. ,krause m. ,flaczyk a. ,möller t.-m. ,tsai m. ,galli s. ,vieths s. ,toda m. ,scheurer s. ,schülke s.
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منبع
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journal of immunology research - 2017 - دوره : 2017 - شماره : 0
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چکیده
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Background. tlr ligands can promote th1-biased immune responses,mimicking potent stimuli of viruses and bacteria. aim. to investigate the adjuvant properties of dual tlr2/7 ligands compared to those of the mixture of both single ligands. methods. dual tlr2/7 ligands: cl401,cl413,and cl531,including cl264 (tlr7-ligand) and pam 2 cysk 4 (tlr2-ligand),were used. immune-modulatory capacity of the dual ligands with the individual ligands alone or as a mixture in mouse bmmdcs,bmmdc:tc cocultures,or bmcmcs was compared and assessed in naïve mice and in a mouse model of ova-induced intestinal allergy. results. cl413 and cl531 induced bmmdc-derived il-10 secretion,suppressed rova-induced il-5 secretion from ova-specific do11.10 cd4 + tcs,and induced proinflammatory cytokine secretion in vivo. in contrast,cl401 induced considerably less il-10 secretion and led to il-17a production in bmmdc:tc cocultures,but not bmcmc il-6 secretion,or il-6 or tnf-α production in vivo. no immune-modulating effects were observed with single ligands. all dual tlr2/7 ligands suppressed dnp-induced ige-and-ag-specific mast cell degranulation. compared to vaccination with ova,vaccination with the mixture cl531 and ova,significantly suppressed ova-specific ige production in the intestinal allergy model. conclusions. based on beneficial immune-modulating properties,cl413 and cl531 may have utility as potential adjuvants for allergy treatment. © 2017 jonathan laiño et al.
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آدرس
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vice president's research group 1,molecular allergology,paul-ehrlich-institut,langen, Germany, vice president's research group 1,molecular allergology,paul-ehrlich-institut,langen, Germany, vice president's research group 1,molecular allergology,paul-ehrlich-institut,langen, Germany, vice president's research group 1,molecular allergology,paul-ehrlich-institut,langen, Germany, vice president's research group 1,molecular allergology,paul-ehrlich-institut,langen, Germany, vice president's research group 1,molecular allergology,paul-ehrlich-institut,langen, Germany, vice president's research group 1,molecular allergology,paul-ehrlich-institut,langen, Germany, department of pathology,sean n. parker center,allergy and asthma research,stanford university,school of medicine,stanford,ca, United States, department of pathology,sean n. parker center,allergy and asthma research,stanford university,school of medicine,stanford,ca,united states,department of microbiology and immunology,stanford university,school of medicine,stanford,ca, United States, vice president's research group 1,molecular allergology,paul-ehrlich-institut,langen, Germany, vice president's research group 1,molecular allergology,paul-ehrlich-institut,langen, Germany, vice president's research group 1,molecular allergology,paul-ehrlich-institut,langen, Germany, vice president's research group 1,molecular allergology,paul-ehrlich-institut,langen, Germany
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Authors
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