The role of indoxyl sulfate, a circulating uremic toxin, for inflammatory responses in the patients with end-stage renal disease (HUM1P.304)

CD16 Pathogenesis CX3CL1 Monocyte
DOI: 10.4049/jimmunol.194.supp.52.29 Publication Date: 2023-01-01T10:37:22Z
ABSTRACT
Abstract In the ESRD patients, a major cause of death is cardiovascular disease (CVD) and its pathologic processes have been suggested to link uremia-related chronic inflammation. Although concept ESRD-related immune dysfunction well-accepted, little known about how uremic toxins affect cellular immunity involved with pathogenesis CVD in patients. Thus, we investigated phenotypic functional features CD4 T cells monocytes patients their responses mediated by indoxyl sulfate (IS), key toxin order explore pathogenic roles these for vascular endothelial (VEC). CD4+CD28null CD16+ were expanded as compared HC. To milieu affects responses, stimulated IS. These produced large amount TNF-α through aryl hydrocarbon receptor. VEC greatly CX3CL1, ligand CX3CR1 which overexpressed monocytes. are preferentially recruited CX3CL1 moreover, cytotoxic capability allowing induced apoptosis response TCR stimulation. Our findings suggest that IS-mediated may play critical role development accelerated progression damage
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