CD4+CD28null cells are expanded and exhibit a cytolytic profile in end-stage renal disease patients on peritoneal dialysis

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Abstract

Background. End-stage renal failure patients, including those on peritoneal dialysis (PD), exhibit several nontraditional cardiovascular (CV) risk factors. A role of CD4+CD28null T lymphocytes in the genesis of coronary artery disease (CAD) has been proposed. We investigated this cell population and examined its phenotype in a cohort of PD patients without CV disease.Methods. The frequency of the peripheral blood CD4+CD28 null T-cell compartment and cytotoxic characteristic of these cells (as assessed by perforin and granzyme B expressions) were determined in 33 PD patients without CAD and 20 healthy subjects by two-and three-color flowcytometry. High-sensitivity C-reactive protein (hs-CRP) was determined by enzyme-linked immunosorbent assay. We investigated whether there was a correlation between these cells and traditional CV risk factors.Results. Compared to healthy controls, CD4+CD28null T cells were significantly expanded in PD patients (10.30 ± 2.03% versus 3.55 ± 0.67%, mean ± SE, P = 0.0007). Perforin and granzyme B expressions were restricted to CD4+CD28null T cells compared to CD4 +CD28+ T cells (<0.0001). A greater proportion of CD4+CD28null T cells in PD patients expressed these molecules (P = 0.007 and 0.04). hs-CRP level was increased in PD patients (P < 0.0001) but did not correlate with the CD4+CD28null T-cell frequency. Increasing age correlated with the CD4+CD28 null cells.Conclusions. PD patients exhibit a substantially increased number of circulating CD4+CD28null T cells that show a cytolytic profile before the onset of clinically significant CAD. Their significance as a nontraditional CV risk factor needs further studies. © 2010 The Author.

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APA

Yadav, A. K., & Jha, V. (2011). CD4+CD28null cells are expanded and exhibit a cytolytic profile in end-stage renal disease patients on peritoneal dialysis. Nephrology Dialysis Transplantation, 26(5), 1689–1694. https://doi.org/10.1093/ndt/gfr010

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