Apoptosis of peripheral CD4++ T-lymphocytes in end-stage renal disease patients under hemodialysis and rhEPO therapies

Ana Borges, Margarida Borges, João Fernandes, Henrique Nascimento, Maria Sameiro-Faria, Vasco Miranda, Flávio Reis, Luis Belo, Elisio Costa*, Alice Santos-Silva

*Autor correspondente para este trabalho

Resultado de pesquisarevisão de pares

20 Citações (Scopus)

Resumo

End-stage renal disease (ESRD) under hemodialyses (HD) is related with a higher propensity to infections, essentially due to T-cell lymphopenia. We postulated that HD procedure affects CD4++ T cells, especially by inducing apoptotic death and that recombinant human erythropoietin (rhEPO) therapy may also play an important role in the modulation of the immune system in these patients. T-cell phenotype and apoptosis of HD patients and healthy controls were evaluated by flow cytometry using anticoagulated whole-blood samples. In 12 HD patients, these parameters were also analyzed before and immediately after HD procedure. HD patients showed a decrease in total circulating CD3++ lymphocytes, especially in CD4++ T cells (0.747 ± 0.410 vs. 0.941 ± 0.216 × 109/L, p < 0.05), which could be a consequence of the higher proportion of CD3 ++ and CD4++ lymphocytes in the latest stage of apoptosis (or death) and of the higher proportion of apoptotic CD4++ T cells observed in the patients immediately after HD procedure (2.91 ± 0.780 vs. 3.90 ± 1.96, p < 0.05). A positive and statistically significant correlation between CD3++ and CD4++ lymphocytes in latest stage of apoptosis (or death) with HD time was found (CD3++: r = 0.592, p < 0.01; CD4++: r = 0.501, p < 0.01). We also found a negative and significant correlation between weekly rhEPO doses and the number of CD4++ T cells (r = -0.358, p < 0.05). In conclusion, HD procedure still contributes to the development of T-cell lymphopenia, at least in part, by apoptosis induction. It was also shown that rhEPO therapy is associated with the CD4++ T-cell decline, possibly by immune modulation, eliminating atypical cells and helping to restore the CD4 ++ T-cell subset.
Idioma originalEnglish
Número do artigo553300
Páginas (de-até)138-143
Número de páginas6
RevistaRenal Failure
Volume33
Número de emissão2
DOIs
Estado da publicaçãoPublished - mar 2011

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