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Immune cell-lipid interaction, a mechanism of CKD-induced accelerated atherosclerosis (M07)

Subject Area Clinical Immunology and Allergology
Term since 2023
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 322900939
 
Patients with CKD show aggravated atherosclerosis and vascular complications. We observed that CKD triggers the post-translational guanidinylation of Apolipoprotein A-I (ApoA-I, the primary protein of HDL), altering ApoA-I from a protective to pro-inflammatory protein. Also, we provided new insights into intestinal integrin-β7+ intraepithelial lymphocytes (IELs), known drivers of atherosclerosis formation. This project now aims to validate targeting of β7+ IELs as a therapeutic approach against CKD-induced accelerated atherosclerosis formation and elucidate the relevance of post-translationally guanidinylated ApoA-I and macrophage interaction.
DFG Programme CRC/Transregios
 
 

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