scholarly journals Lymph node and circulating T cell characteristics are strongly correlated in end-stage renal disease patients, but highly differentiated T cells reside within the circulation

2017 ◽  
Vol 188 (2) ◽  
pp. 299-310 ◽  
Author(s):  
B. Dedeoglu ◽  
A. E. de Weerd ◽  
L. Huang ◽  
A. W. Langerak ◽  
F. J. Dor ◽  
...  
Keyword(s):  
T Cells ◽  
Lymph Node ◽  
T Cell ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Strongly Correlated ◽  
Stage Renal Disease ◽  
End Stage

scholarly journals Peptide Vaccination against Cytomegalovirus Induces Specific T Cell Response in Responses in CMV Seronegative End-Stage Renal Disease Patients

Vaccines ◽  
2021 ◽  
Vol 9 (2) ◽  
pp. 133
Author(s):  
Claudia Sommerer ◽  
Anita Schmitt ◽  
Angela Hückelhoven-Krauss ◽  
Thomas Giese ◽  
Thomas Bruckner ◽  
...  
Keyword(s):  
T Cells ◽  
Kidney Transplantation ◽  
T Cell ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Solid Organ ◽  
Peptide Vaccination ◽  
Stage Renal Disease ◽  
End Stage ◽  
Cmv Reactivation

Introduction: Cytomegalovirus (CMV) reactivation occurs in seronegative patients after solid organ transplantation (SOT) particularly from seropositive donors and can be lethal. Generation of CMV-specific T cells helps to prevent CMV reactivation. Therefore, we initiated a clinical phase I CMVpp65 peptide vaccination trial for seronegative end-stage renal disease patients waiting for kidney transplantation. Methods: The highly immunogenic nonamer peptide NLVPMVATV derived from CMV phosphoprotein 65(CMVpp65) in a water-in-oil emulsion (Montanide™) plus imiquimod (Aldara™) as an adjuvant was administered subcutaneously four times biweekly. Clinical course as well as immunological responses were monitored using IFN-γ ELISpot assays and flow cytometry for CMV-specific CD8+ T cells. Results: Peptide vaccination was well tolerated, and no drug-related serious adverse events were detected except for Grade I–II local skin reactions. Five of the 10 patients (50%) mounted any immune response (responders) and 40% of the patients presented CMV-specific CD8+ T cell responses elicited by these prophylactic vaccinations. No responders experienced CMV reactivation in the 18 months post-transplantation, while all non-responders reactivated. Conclusion: CMVpp65 peptide vaccination was safe, well tolerated, and clinically encouraging in seronegative end-stage renal disease patients waiting for kidney transplantation. Further studies with larger patient cohorts are planned.

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

2021 ◽  
Vol 22 (6) ◽  
pp. 2975
Author(s):  
Erasmia Sampani ◽  
Dimitra-Vasilia Daikidou ◽  
George Lioulios ◽  
Aliki Xochelli ◽  
Zoi Mitsoglou ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
T Cells ◽  
T Cell ◽  
Regulatory T Cells ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Cell Immunity ◽  
Stage Renal Disease ◽  
End Stage ◽  
Esrd Patients

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.

scholarly journals End-stage renal disease, dialysis, kidney transplantation and their impact on CD4+T-cell differentiation

Immunology ◽  
2018 ◽  
Vol 155 (2) ◽  
pp. 211-224 ◽  
Author(s):  
Matthias Schaier ◽  
Angele Leick ◽  
Lorenz Uhlmann ◽  
Florian Kälble ◽  
Christian Morath ◽  
...  
Keyword(s):  
Kidney Transplantation ◽  
Cell Differentiation ◽  
T Cell ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
T Cell Differentiation ◽  
Cd4 T Cell ◽  
Stage Renal Disease ◽  
End Stage

scholarly journals End stage renal disease patients have a skewed T cell receptor Vβ repertoire

2015 ◽  
Vol 12 (1) ◽  
Author(s):  
Ling Huang ◽  
Anton W. Langerak ◽  
Ingrid L. M. Wolvers-Tettero ◽  
Ruud W. J. Meijers ◽  
Carla C. Baan ◽  
...  
Keyword(s):  
T Cell ◽  
Renal Disease ◽  
T Cell Receptor ◽  
End Stage Renal Disease ◽  
Cell Receptor ◽  
Stage Renal Disease ◽  
End Stage ◽  
T Cell Receptor Vβ

Ex vivo expanded natural regulatory T cells from patients with end-stage renal disease or kidney transplantation are useful for autologous cell therapy

2018 ◽  
Vol 93 (6) ◽  
pp. 1452-1464 ◽  
Author(s):  
Sybille Landwehr-Kenzel ◽  
Anne Zobel ◽  
Henrike Hoffmann ◽  
Niels Landwehr ◽  
Michael Schmueck-Henneresse ◽  
...  
Keyword(s):  
T Cells ◽  
Kidney Transplantation ◽  
Cell Therapy ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Ex Vivo ◽  
Autologous Cell ◽  
Autologous Cell Therapy ◽  
Stage Renal Disease ◽  
End Stage

T-cell aging in end-stage renal disease: an evolving story with CMV

2019 ◽  
Vol 208 (3-4) ◽  
pp. 281-287 ◽  
Author(s):  
TienYu Owen Yang ◽  
Yi-Fang Chuang ◽  
Yen-Ling Chiu
Keyword(s):  
T Cell ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Cell Aging ◽  
Stage Renal Disease ◽  
End Stage

Erythrocyte Adhesion in Hemodialysis Patients – A Novel Potential Contributor to Inflammation in End-Stage Renal Disease.

Blood ◽  
2012 ◽  
Vol 120 (21) ◽  
pp. 2092-2092
Author(s):  
Vimal K. Derebail ◽  
Adam McDonald ◽  
Julia Brittain
Keyword(s):  
T Cells ◽  
Endothelial Cells ◽  
Renal Disease ◽  
Sickle Cell ◽  
End Stage Renal Disease ◽  
Sickle Cell Trait ◽  
Hemodialysis Patients ◽  
Healthy Control ◽  
Stage Renal Disease ◽  
End Stage

Abstract Abstract 2092 Background: Widespread adhesion of erythrocytes in the vasculature would be incompatible with life. However, in illnesses such as sickle cell disease, malaria and diabetes, adhesive RBCs have been documented and are likely contributors to disease severity, inflammation and coagulation activation. End-stage renal disease is characterized by profound, global inflammation and relative thrombophilia. While we, and others, have reported the extensive exposure of RBC phosphatidylserine in patients on hemodialysis, the role of RBC adhesion in inflammation has never been examined in this condition. We performed an analysis of RBCs from hemodialysis patients to characterize their ability to adhere to other cells, elucidate the potential mechanisms of adhesion, and to relate RBC adhesion to the inflammatory state of hemodialysis. Methods: This study was conducted in a cohort of 20 African American patients receiving in-center hemodialysis at 2 separate dialysis clinics as part of a study of sickle cell trait in hemodialysis. There were 9 of 20 patients with documented sickle cell trait. Blood samples were drawn immediately pre-dialysis and prior to administration of heparin. Plasma samples were processed to minimize platelet activation, aliquoted, and frozen for batch analysis. Plasma factors (RANTES, CRP & CD40L) were analyzed via ELISA. Adhesion events in whole blood were detected via two color flow cytometry. Cause of renal failure, mode of venous access and relevant clinical data were obtained from patient charts. All adhesion assays with washed blood cells were conducted under static conditions using microvascular endothelial cells. All studies were compared to those results of healthy control patients (n =11). Spearman's regression analysis was performed to analyze the correlation between continuous variables. Mann-Whitney U and Kruskal Wallis tests were used to compare continuous variables between groups. A p<0.05 was considered significant. Results: We found that RBCs from patients on hemodialysis were significantly more adhesive than those from healthy controls. In whole blood, we detected marked RBC adhesion to T-cells (median % of T-cells bound to RBCs: 67.9 [hemodialysis] vs. 10.55 [healthy control]) and platelets (median % of platelets bound to RBCs: 33.0 vs. 1.1%). We also noted significant RBC adhesion to neutrophils (median % of neutrophils bound to RBCs: 11.0% vs. 0.1%). Incubation of healthy RBCs with plasma from hemodialysis patients, but not healthy control plasma, was sufficient to induce RBC adhesion to cultured endothelial cells (median RBCs/mm2: 8.0 vs. 0.5) and to T-cells (median % T-cells bound to RBCs: 30.0 vs. 5.0). Plasma from hemodialysis patients also induced phosphatidylserine exposure on healthy RBCs. Phosphatidylserine exposure on the RBC appeared to mediate RBC adhesion to endothelial cells as annexin V significantly reduced RBC adherence (8.0 vs 3.8 RBC/mm2). The extent to which RBCs in hemodialysis patients adhered to T-cells directly correlated with both plasma RANTES (rspearman = 0.65, 95% CI: 0.247–0.864) and CD40L levels (rspearman= 0.60, 95% CI: 0.1645 – 0.847), but not plasma CRP levels. There was also no significant difference in adhesion of RBCs due to cause of renal failure (diabetes, hypertension, or glomerulonephritis) or presence of sickle cell trait. Conclusions: We describe for the first time a novel adhesion of RBCs in patients receiving hemodialysis and how this adhesion may relate to inflammation in these patients. Our findings also suggest that factors in uremic plasma are sufficient to induce phosphatidylserine exposure on RBCs. This exposure, in addition to providing a site for thrombin generation, also serves as an adhesive moiety on RBCs for endothelial cells. These data may describe an unrecognized etiology of inflammation in hemodialysis and end-stage renal disease. Disclosures: No relevant conflicts of interest to declare.

Influence of end stage renal disease on CD28 expression and T‐cell immunity

Nephrology ◽  
2020 ◽  
Author(s):  
Erasmia Sampani ◽  
Maria Stangou ◽  
Dimitra‐Vasilia Daikidou ◽  
Vasiliki Nikolaidou ◽  
Despoina Asouchidou ◽  
...  
Keyword(s):  
T Cell ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
T Cell Immunity ◽  
Cell Immunity ◽  
Stage Renal Disease ◽  
End Stage
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