T cell markers recount the course of immunosenescence in healthy individuals and chronic kidney disease

Λιούλιος, Γεώργιος; Fylaktou, Asimina; Papagianni, Aikaterini; Stangou, Μaria

doi:10.1016/j.clim.2021.108685

Cited by 26 publications

(40 citation statements)

References 144 publications

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“…Chronic metabolic acidosis, oxidative stress, the accumulation of uremic toxins, and low-grade inflammation are some of the consequences of end-stage renal disease (ESRD) [1][2][3]. They directly affect almost every system, including the immune system, which is the overarching surveillance mechanism to control almost each function [4,5]. Immunological complications in chronic kidney disease encompass the exceptional characteristic of combined immune deficiency happening together with chronic inflammation [4,6,7].…”

Section: Introductionmentioning

confidence: 99%

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CD28null and Regulatory T Cells Are Substantially Disrupted in Patients with End-Stage Renal Disease Due to Diabetes Mellitus

Sampani

Daikidou

Lioulios

et al. 2021

IJMS

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Background: End-stage renal disease (ESRD) is associated with alterations in T-cell immunity, including increased CD28null and reduced regulatory T cells (Tregs). However, whether immune disturbances are due to ESRD or primary disease is not yet clear. As diabetes mellitus is the leading cause of ESRD, we evaluated its impact on the immune profile of ESRD patients. Methods: CD28null, Tregs, and natural killer cells were initially analyzed by flow cytometry in 30 predialysis ESRD patients due to diabetes (DM), 30 non-DM (NDM), and 25 healthy controls. Measurements were repeated after 6 months on hemodialysis (HD) or peritoneal dialysis (CAPD). Results: The percentage of CD4 + CD28null cells, CD8 + CD28null cells, and Tregs showed significant differences in DM, NDM, and controls; mean rank 33.71 vs. 25.68 vs. 18.88, p = 0.006, 37.79 vs. 28.82 vs. 17.08, p = 0.008, and 20.79 vs. 26.12 vs. 41.33, p = 0.001, respectively. DM vs. NDM had increased CD4 + CD28null and CD8 + CD28null cells, 11.5% (1.5%–24%) vs. 4.1% (0–42.3%), p = 0.02 and 61.3% (24%–76%) vs. 43% (5.7%–85%), p = 0.04, respectively. After 6 months on HD but not CAPD, DM showed a significant further increase in CD4 + CD28null cells, from 30 (14–100) to 52.7 (15–203), p = 0.02; and CD8 + CD28null cells, from 137 (56–275) to 266 (103–456), p = 0.01. Conclusions: Diabetes mellitus affects T-cell subtypes even at predialysis stage, though changes become more prominent after commencement on HD.

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Section: Introductionmentioning

confidence: 99%

“…They directly affect almost every system, including the immune system, which is the overarching surveillance mechanism to control almost each function [4,5]. Immunological complications in chronic kidney disease encompass the exceptional characteristic of combined immune deficiency happening together with chronic inflammation [4,6,7].…”

Section: Introductionmentioning

confidence: 99%

CD28null and Regulatory T Cells Are Substantially Disrupted in Patients with End-Stage Renal Disease Due to Diabetes Mellitus

Sampani

Daikidou

Lioulios

et al. 2021

IJMS

Self Cite

View full text Add to dashboard Cite

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“…Although metabolic and hemodynamic disorders are considered to predominate in the pathogenesis of both conditions, recent accumulating evidence emphasizes the causative role of immune mechanisms. Immunological disorders in CKD are usually the result of impaired renal function per se, which seems to affect both cell and humoral immunity, leading to alterations in T and B cell phenotype and activation of inflammatory cells, phenomena implicated in the development of cardiovascular disease [22,23].…”

Section: Discussionmentioning

confidence: 99%

Histology and Immunohistochemistry of Radial Arteries Are Suggestive of an Interaction between Calcification and Early Atherosclerotic Lesions in Chronic Kidney Disease

et al. 2021

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Background and Objectives: recent studies suggest an implication of immune mechanisms in atherosclerotic disease. In this paper, the interaction between inflammation, calcification, and atherosclerosis on the vessel walls of patients with chronic kidney disease (CKD) is described and evaluated. Materials and Methods: patients with stage V CKD, either on pre-dialysis (group A) or on hemodialysis (HD) for at least 2 years (group B), in whom a radiocephalic arteriovenous fistula (RCAVF) was created, were included in the study. The control group included healthy volunteers who received radial artery surgery after an accident. The expressions of inflammatory cells, myofibroblasts, and vascular calcification regulators on the vascular wall were estimated, and, moreover, morphometric analysis was performed. Results: the expressions of CD68(+) cells, matrix carboxyglutamic acid proteins (MGPs), the receptor activator of nuclear factor-kB (RANK) and RANK ligand (RANKL), and osteoprotegerin (OPG), were significantly increased in CKD patients compared to the controls p = 0.02; p = 0.006; p = 0.01; and p = 0.006, respectively. In morphometric analysis, the I/M and L/I ratios had significant differences between CKD patients and the controls 0.3534 ± 0.20 vs. 0.1520 ± 0.865, p = 0.003, and 2.1709 ± 1.568 vs. 4.9958 ± 3.2975, p = 0.03, respectively. The independent variables correlated with the degree of vascular calcification were the intensity of CD34(+), aSMA(+) cells, and OPG, R2 = 0.76, p < 0.0001, and, with intima-media thickness (IMT), the severity of RANKL expression R2 = 0.3, p < 0.0001. Conclusion: atherosclerosis and vascular calcification in CKD seem to be strongly regulated by an immunological and inflammatory activation on the vascular wall.

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“…Several other surface molecules were validated as markers of senescence by other studies including TNFRSF10D/CD264 [ 56 ], NOTCH1 [ 57 ], NOTCH3 [ 58 ], CD36 [ 59 ], oxidized Vimentin [ 60 ], ICAM-1 [ 12 ], and uPAR [ 61 ]. More recently, it was proposed that a broad range of surface markers can be used to identify immunosenescent T-cells in chronic kidney disease [ 62 ]. Finally, immunomodulatory signals and surface markers on mesenchymal stem cells (MSCs) were shown to be differentially expressed between old and young mice [ 63 , 64 ].…”

Section: The Emergence Of Surface Proteins As Biomarkers and Therapeutic Targetsmentioning

confidence: 99%

The Emergence of Senescent Surface Biomarkers as Senotherapeutic Targets

Rossi

Abdelmohsen

2021

Cells

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Senescence is linked to a wide range of age-associated diseases and physiological declines. Thus, senotherapeutics are emerging to suppress the detrimental effects of senescence either by senomorphics or senolytics. Senomorphics suppress the traits associated with senescence phenotypes, while senolytics aim to clear senescent cells by suppressing their survival and enhancing the apoptotic pathways. The main goal of these approaches is to suppress the proinflammatory senescence-associated secretory phenotype (SASP) and to promote the immune recognition and elimination of senescent cells. One increasingly attractive approach is the targeting of molecules or proteins specifically present on the surface of senescent cells. These proteins may play roles in the maintenance and survival of senescent cells and hence can be targeted for senolysis. In this review, we summarize the recent knowledge regarding senolysis with a focus on novel surface biomarkers of cellular senescence and discuss their emergence as senotherapeutic targets.

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T cell markers recount the course of immunosenescence in healthy individuals and chronic kidney disease

Cited by 26 publications

References 144 publications

CD28null and Regulatory T Cells Are Substantially Disrupted in Patients with End-Stage Renal Disease Due to Diabetes Mellitus

CD28null and Regulatory T Cells Are Substantially Disrupted in Patients with End-Stage Renal Disease Due to Diabetes Mellitus

Histology and Immunohistochemistry of Radial Arteries Are Suggestive of an Interaction between Calcification and Early Atherosclerotic Lesions in Chronic Kidney Disease

The Emergence of Senescent Surface Biomarkers as Senotherapeutic Targets

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