<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>9</volume><submitter>Kumawat AK</submitter><pubmed_abstract>The balance between pro- and anti-inflammatory cytokines released by immune and non-immune cells plays a decisive role in the progression of atherosclerosis. Interleukin (IL)-17A has been shown to accelerate atherosclerosis. In this study, we investigated the effect on pro-inflammatory mediators and atherosclerosis development of an Affibody molecule that targets IL17A. Affibody molecule neutralizing IL17A, or sham were administered &lt;i>in vitro&lt;/i> to human aortic smooth muscle cells (HAoSMCs) and murine NIH/3T3 fibroblasts and &lt;i>in vivo&lt;/i> to atherosclerosis-prone, hyperlipidaemic ApoE&lt;sup>-/-&lt;/sup> mice. Levels of mediators of inflammation and development of atherosclerosis were compared between treatments. Exposure of human smooth muscle cells and murine NIH/3T3 fibroblasts &lt;i>in vitr</pubmed_abstract><journal>Frontiers in cardiovascular medicine</journal><pagination>831039</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC8907570</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Inhibition of IL17A Using an Affibody Molecule Attenuates Inflammation in ApoE-Deficient Mice.</pubmed_title><pmcid>PMC8907570</pmcid><pubmed_authors>Soderstrom LA</pubmed_authors><pubmed_authors>Caravaca AS</pubmed_authors><pubmed_authors>Sirsjo A</pubmed_authors><pubmed_authors>Baumgartner R</pubmed_authors><pubmed_authors>Gistera A</pubmed_authors><pubmed_authors>Ketelhuth DFJ</pubmed_authors><pubmed_authors>Hellberg S</pubmed_authors><pubmed_authors>Zegeye MM</pubmed_authors><pubmed_authors>Jin H</pubmed_authors><pubmed_authors>Ljungberg LU</pubmed_authors><pubmed_authors>Frejd FY</pubmed_authors><pubmed_authors>Amegavie O</pubmed_authors><pubmed_authors>Kumawat AK</pubmed_authors><pubmed_authors>Gudmundsdotter L</pubmed_authors><pubmed_authors>Olofsson PS</pubmed_authors><pubmed_authors>Paramel GV</pubmed_authors></additional><is_claimable>false</is_claimable><name>Inhibition of IL17A Using an Affibody Molecule Attenuates Inflammation in ApoE-Deficient Mice.</name><description>The balance between pro- and anti-inflammatory cytokines released by immune and non-immune cells plays a decisive role in the progression of atherosclerosis. Interleukin (IL)-17A has been shown to accelerate atherosclerosis. In this study, we investigated the effect on pro-inflammatory mediators and atherosclerosis development of an Affibody molecule that targets IL17A. Affibody molecule neutralizing IL17A, or sham were administered &lt;i>in vitro&lt;/i> to human aortic smooth muscle cells (HAoSMCs) and murine NIH/3T3 fibroblasts and &lt;i>in vivo&lt;/i> to atherosclerosis-prone, hyperlipidaemic ApoE&lt;sup>-/-&lt;/sup> mice. Levels of mediators of inflammation and development of atherosclerosis were compared between treatments. Exposure of human smooth muscle cells and murine NIH/3T3 fibroblasts &lt;i>in vitr</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022</publication><modification>2025-04-25T23:02:08.987Z</modification><creation>2025-04-06T09:13:56.031Z</creation></dates><accession>S-EPMC8907570</accession><cross_references><pubmed>35282365</pubmed><doi>10.3389/fcvm.2022.831039</doi></cross_references></HashMap>