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ArticleInflammation research : official journal of the European Histamine Research Society ... [et al.]2024

Characteristics of T cell premature senescence in maintenance hemodialysis patients.

Wangshu Wu, Ahui Song, Kewei Xie, Jiayue Lu, Bingru Zhao, Cheng Qian, Minzhou Wang, Lulin Min, Wenkai Hong, Huihua Pang and 2 more

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Article in Inflammation research : official journal of the European Histamine Research Society ... [et al.], 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

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3 · Its place in the literature

Who cites it

6 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

12 authors.

Wangshu Wu *Department of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Renji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, 160# Pujian Road, Building 1, 2nd Floor, Shanghai, 200127, China.
Ahui Song *Department of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Renji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, 160# Pujian Road, Building 1, 2nd Floor, Shanghai, 200127, China.
Kewei Xie *Department of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Renji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, 160# Pujian Road, Building 1, 2nd Floor, Shanghai, 200127, China.
Jiayue LuDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Renji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, 160# Pujian Road, Building 1, 2nd Floor, Shanghai, 200127, China.
Bingru ZhaoDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Renji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, 160# Pujian Road, Building 1, 2nd Floor, Shanghai, 200127, China.
Cheng QianDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Renji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, 160# Pujian Road, Building 1, 2nd Floor, Shanghai, 200127, China.
Minzhou WangDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Renji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, 160# Pujian Road, Building 1, 2nd Floor, Shanghai, 200127, China.
Lulin MinDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Renji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, 160# Pujian Road, Building 1, 2nd Floor, Shanghai, 200127, China.
Wenkai HongDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Renji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, 160# Pujian Road, Building 1, 2nd Floor, Shanghai, 200127, China.
Huihua PangDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Renji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, 160# Pujian Road, Building 1, 2nd Floor, Shanghai, 200127, China. panghuihua@126.com.
Renhua LuDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Renji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, 160# Pujian Road, Building 1, 2nd Floor, Shanghai, 200127, China. lurenhua1977@hotmail.com.
Leyi GuDepartment of Nephrology, Molecular Cell Lab for Kidney Disease, Shanghai Peritoneal Dialysis Research Center, Renji Hospital, Uremia Diagnosis and Treatment Center, Shanghai Jiao Tong University School of Medicine, 160# Pujian Road, Building 1, 2nd Floor, Shanghai, 200127, China. guleyi@aliyun.com.

Funding

National Natural Science Foundation of China 81970610National Natural Science Foundation of China 82000634Program of Shanghai Academic/Technology Research Leader 22XD1431400Shanghai Municipal Education Commission Gaofeng Clinical Medicine Grant 20172015Shanghai Sailing Program 20YF1425000Shanghai Science/Technology Commission/Animal Special Program 22140903900
6 · The paper itself

Abstract

backgroundUremia-associated immunodeficiency, mainly characterized by T cell dysfunction, exists in patients on maintenance hemodialysis (MHD) and promotes systemic inflammation. However, T cell senescence, one of the causes of T cell dysfunction, has not been clearly revealed yet. In this cross-sectional research, we aimed to study the manifestation of T cell premature senescence in MHD patients and further investigate the associated clinical factors.

methods76 MHD patients including 33 patients with cardiovascular diseases (CVD) and 28 patients with arteriovenous fistula (AVF) event history were enrolled in this study. Complementarity determining region 3 (CDR3) of T cell receptor (TCR) was analyzed by immune repertoire sequencing (IR-Seq). CD28- T cell subsets and expression of senescence marker p16 and p21 genes were detected by multicolor flow cytometry and RT-qPCR, respectively.

resultsMHD patients had significantly decreased TCR diversity (P < 0.001), increased CDR3 clone proliferation (P = 0.001) and a left-skewed CDR3 length distribution. The proportion of CD4 + CD28- T cells increased in MHD patients (P = 0.014) and showed a negative correlation with TCR diversity (P = 0.001). p16 but not p21 expression in T cells was up-regulated in MHD patients (P = 0.039). Patients with CVD exhibited increased expression of p16 and p21 genes (P = 0.010 and 0.004, respectively), and patients with AVF events showed further TCR diversity and evenness reduction (P = 0.002 and 0.017, respectively) compared to patients without the comorbidities. Moreover, age, average convection volume, total cholesterol, high-density lipoprotein cholesterol and transferrin saturation were associated with TCR diversity or CD4 + CD28- T cell proportion (P < 0.05).

conclusionsMHD patients undergo T cell premature senescence characterized by significant TCR diversity reduction and repertoire skew, as well as accumulation of the CD4 + CD28- subset and up-regulation of p16 gene. Patients with CVD or AVF events show higher level of immunosenescence. Furthermore, T cell senescence in MHD patients is associated with blood cholesterol and uremic toxin retention, suggesting potential intervention strategies in the future.

Indexed as

Cellular SenescenceReceptors, Antigen, T-CellRenal DialysisAdultAgedCardiovascular DiseasesCD28 AntigensCD4-Positive T-LymphocytesComplementarity Determining RegionsCross-Sectional StudiesCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21FemaleHumansMaleMiddle AgedCD28 AntigensCDKN1A protein, humanCDKN2A protein, humanComplementarity Determining RegionsCyclin-Dependent Kinase Inhibitor p16Cyclin-Dependent Kinase Inhibitor p21Receptors, Antigen, T-CellHemodialysisImmunosenescenceInflammagingInflammationT-cell receptorT-lymphocytes

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.