{"database":"biostudies-literature","file_versions":[],"scores":null,"additional":{"submitter":["Wolf D"],"funding":["NHLBI NIH HHS"],"pagination":["1269-79"],"full_dataset_link":["https://www.ebi.ac.uk/biostudies/studies/S-EPMC3291815"],"repository":["biostudies-literature"],"omics_type":["Unknown"],"volume":["109(11)"],"pubmed_abstract":["<h4>Rationale</h4>CD40L figures prominently in chronic inflammatory diseases such as atherosclerosis. However, since CD40L potently regulates immune function and hemostasis by interaction with CD40 receptor and the platelet integrin GPIIb/IIIa, its global inhibition compromises host defense and generated thromboembolic complications in clinical trials. We recently reported that CD40L mediates atherogenesis independently of CD40 and proposed Mac-1 as an alternate receptor.<h4>Objective</h4>Here, we molecularly characterized the CD40L-Mac-1 interaction and tested whether its selective inhibition by a small peptide modulates inflammation and atherogenesis in vivo.<h4>Methods and results</h4>CD40L concentration-dependently bound to Mac-1 I-domain in solid phase binding assays, and a high-affin"],"journal":["Circulation research"],"pubmed_title":["Binding of CD40L to Mac-1's I-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis--but does not affect immunity and thrombosis in mice."],"pmcid":["PMC3291815"],"funding_grant_id":["R01 HL061589","R01 HL034636","HL 34636","R37 HL034636"],"pubmed_authors":["Wiedemann A","Hoppe N","Stachon P","von zur Muhlen C","Blankenbach H","Duerschmied D","Zeschky K","Rodriguez AO","Peter K","Bassler N","Herr N","Soloviev DA","Zhang L","Plow EF","Hilgendorf I","Zirlik A","Wolf D","Marchini T","Bledzka K","Willecke F","Libby P","Gutte K","Hohmann JD","Bode C"],"additional_accession":[]},"is_claimable":false,"name":"Binding of CD40L to Mac-1's I-domain involves the EQLKKSKTL motif and mediates leukocyte recruitment and atherosclerosis--but does not affect immunity and thrombosis in mice.","description":"<h4>Rationale</h4>CD40L figures prominently in chronic inflammatory diseases such as atherosclerosis. However, since CD40L potently regulates immune function and hemostasis by interaction with CD40 receptor and the platelet integrin GPIIb/IIIa, its global inhibition compromises host defense and generated thromboembolic complications in clinical trials. We recently reported that CD40L mediates atherogenesis independently of CD40 and proposed Mac-1 as an alternate receptor.<h4>Objective</h4>Here, we molecularly characterized the CD40L-Mac-1 interaction and tested whether its selective inhibition by a small peptide modulates inflammation and atherogenesis in vivo.<h4>Methods and results</h4>CD40L concentration-dependently bound to Mac-1 I-domain in solid phase binding assays, and a high-affin","dates":{"release":"2011-01-01T00:00:00Z","publication":"2011 Nov","modification":"2026-04-30T20:58:08.21Z","creation":"2019-03-27T00:49:42Z"},"accession":"S-EPMC3291815","cross_references":{"pubmed":["21998326"],"doi":["10.1161/CIRCRESAHA.111.247684","10.1161/circresaha.111.247684"]}}