BMC nephrology · 2025
Immunomodulatory effect of CD71+ erythroid cells in patients with kidney failure.
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Zamani Batool, Riazian Fatemeh, Taba Masoud Moeini, Namdar Afshin, Barzoki Fateme Zareei, Atapour Abdolamir, Motedayyen Hossein
Аннотация
BACKGROUND: Immune abnormalities play a critical role in the pathogenesis of kidney failure. CD71+ erythroid cells are known to modulate immune responses. However, their immunomodulatory effects in kidney failure patients remain unclear. Therefore, we investigated the frequencies of CD71 + erythroid cells, Th1, Th2, Th17 cells, and regulatory T cells (Tregs), as well as the impact of CD71 + erythroid cells on the proliferation of peripheral blood mononuclear cells (PBMCs) of kidney failure patients.
METHODS: PBMCs were isolated from 49 kidney failure patients and 20 healthy subjects. The frequencies of T cell subsets and CD71 + erythroid cells were determined by flow cytometry. The numbers of reticulocytes and RBCs were also measured. Panel-reactive antibodies screening was used to assess antibodies against human leukocyte antigens (HLAs) in the patients. The effect of CD71 + erythroid cells on PBMC proliferation in kidney failure patients was investigated using a CFSE labeling assay. Erythropoietin level was measured by ELISA.
RESULTS: Kidney failure patients showed a significant increase in CD71 + erythroid cells (P < 0.01). In contrast, the frequencies of Th1, Th2, and Th17 cells were significantly reduced in these patients (P < 0.01-0.05). Among CD4 + T subsets, Th1 cell frequency was inversely correlated with the number of CD71 + erythroid cells (P < 0.05). In vitro, CD71 + erythroid cells inhibited the proliferation of PMBCs in kidney failure patients (P < 0.0001-0.05). No significant difference was observed in Treg frequencies between patients and controls. The frequency of CD71 + erythroid cells was significantly decreased in kidney failure patients with anti-HLA antibodies, unlike patients without anti-HLA antibodies (P < 0.001). The patients had an increased number of reticulocytes, unlike RBC, in peripheral blood compared with healthy subjects (P < 0.01-0.05). The patients exhibited a reduction in erythropoietin level compared with the control group (P < 0.0001).
CONCLUSION: These findings suggest CD71 + erythroid cells may contribute to immune dysregulation in kidney failure patients, potentially playing a role in disease progression and its immunopathology.
METHODS: PBMCs were isolated from 49 kidney failure patients and 20 healthy subjects. The frequencies of T cell subsets and CD71 + erythroid cells were determined by flow cytometry. The numbers of reticulocytes and RBCs were also measured. Panel-reactive antibodies screening was used to assess antibodies against human leukocyte antigens (HLAs) in the patients. The effect of CD71 + erythroid cells on PBMC proliferation in kidney failure patients was investigated using a CFSE labeling assay. Erythropoietin level was measured by ELISA.
RESULTS: Kidney failure patients showed a significant increase in CD71 + erythroid cells (P < 0.01). In contrast, the frequencies of Th1, Th2, and Th17 cells were significantly reduced in these patients (P < 0.01-0.05). Among CD4 + T subsets, Th1 cell frequency was inversely correlated with the number of CD71 + erythroid cells (P < 0.05). In vitro, CD71 + erythroid cells inhibited the proliferation of PMBCs in kidney failure patients (P < 0.0001-0.05). No significant difference was observed in Treg frequencies between patients and controls. The frequency of CD71 + erythroid cells was significantly decreased in kidney failure patients with anti-HLA antibodies, unlike patients without anti-HLA antibodies (P < 0.001). The patients had an increased number of reticulocytes, unlike RBC, in peripheral blood compared with healthy subjects (P < 0.01-0.05). The patients exhibited a reduction in erythropoietin level compared with the control group (P < 0.0001).
CONCLUSION: These findings suggest CD71 + erythroid cells may contribute to immune dysregulation in kidney failure patients, potentially playing a role in disease progression and its immunopathology.