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Altered monocyte-derived dendritic cell function in patients on hemodialysis: a culprit for underlying impaired immune responses
Background Patients with end-stage renal disease (ESRD) are known to have impaired immune function. Dendritic cells (DCs) are the major antigen-presenting cells that initiate primary immune responses, linking innate and adaptive immunity. Although suboptimal immune responses to vaccination, as frequ...
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Published in: | Clinical and experimental nephrology 2011-08, Vol.15 (4), p.546-553 |
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Main Authors: | , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Background
Patients with end-stage renal disease (ESRD) are known to have impaired immune function. Dendritic cells (DCs) are the major antigen-presenting cells that initiate primary immune responses, linking innate and adaptive immunity. Although suboptimal immune responses to vaccination, as frequently observed in ESRD patients, might suggest the presence of impaired DC function, the precise nature of altered DC function is not fully understood.
Methods
In the current study, we compared the maturation status, viability, and function of monocyte-derived DCs (moDCs) of patients on hemodialysis (HD) with healthy controls.
Results
Surface expression of major histocompatibility complex class II, CD83, and CD86, and chemokine receptor CCR7 in moDCs was not different between HD patients and healthy controls. No significant difference was detected in the viability of moDCs determined by expression of annexin V and propidium iodide between two groups. However, moDCs from HD patients produced significantly higher amounts of IL-6 when stimulated by cytokine cocktails compared to healthy controls. In addition, mature moDCs from HD patients showed significantly enhanced allogeneic T-cell proliferation compared to healthy controls.
Conclusions
Our data demonstrate aberrant DC function in HD patients and suggest that this might contribute to impaired immune responses. |
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ISSN: | 1342-1751 1437-7799 |
DOI: | 10.1007/s10157-011-0424-2 |