Decreased CD3+CD16+ natural killer-like T-cell percentage and zeta-chain expression accompany chronic inflammation in haemodialysis patients
- PMID: 19486472
- DOI: 10.1111/j.1440-1797.2008.01041.x
Decreased CD3+CD16+ natural killer-like T-cell percentage and zeta-chain expression accompany chronic inflammation in haemodialysis patients
Abstract
Aim: Clinical and experimental data indicate a deficient immune response in haemodialysis (HD) patients. Natural killer-like (NKL) T cells express on their surface both the T-cell antigen receptor (TCR) and a diverse set of NK-cell receptors (NKR) and share properties of both T cells and NK cells. zeta-Chain phosphorylation is an early event that follows TCR activation or some NKR activation. The zeta-chain of both T cell and NK cells is downregulated in many chronic inflammatory states, HD included. In the present study, NKL T-cell percentage and zeta-chain expression in HD patients were evaluated.
Methods: Thirty-three stable HD patients and 30 healthy volunteers were enrolled into the study. NKL T-cell percentage and NKL T-cell zeta-chain mean fluorescence intensity (MFI) were evaluated with flow cytometry. The inflammatory markers C-reactive protein, interleukin-6 and tumour necrosis factor-alpha were measured in the serum by means of enzyme-linked immunosorbent assay.
Results: All the evaluated markers of inflammation were increased in HD patients. In these patients, NKL T-cell percentage (1.71 +/- 1.69% vs 3.94 +/- 3.86%) and zeta-chain MFI (3.66 +/- 2.79 vs 7.03 +/- 7.91) were decreased.
Conclusions: NKL T-cell percentage and zeta-chain expression is decreased in HD patients. Taking into consideration the continuously increasing age of the HD patients and that normally NKL T-cell numbers increase with age counteracting the impaired T-cell and NK-cell function accompanying advancing age, the above NKL T-cell disturbances could contribute to the impaired immune response in this population. Measures towards alleviating chronic inflammation could partially restore NKL T-cell impairment.
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