ArticleJournal of the American Society of Nephrology : JASN2009
Proteasomal processing of albumin by renal dendritic cells generates antigenic peptides.
Article in Journal of the American Society of Nephrology : JASN, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed.
- Article
- Tubulointerstitial inflammation and fibrosis induced by proteinuria: fresh insights.Frontiers in pharmacology · 2026Review
- Abatacept Decreases Renal T-cell Infiltration and Renal Inflammation and Ameliorates Progressive Renal Injury in Obese Dahl Salt-sensitive Rats Before Puberty.Journal of cardiovascular pharmacology · 2024Article
- Tubulointerstitial injury in proteinuric chronic kidney diseases.Frontiers in medicine · 2024Review
- New-Onset Acute Interstitial Nephritis Post-SARS-CoV-2 Infection and COVID-19 Vaccination: A Panoramic Review.Journal of epidemiology and global health · 2023Review
- Metformin reduces insulin resistance and attenuates progressive renal injury in prepubertal obese Dahl salt-sensitive rats.American journal of physiology. Renal physiology · 2023Article
- Nutritional Treatment as a Synergic Intervention to Pharmacological Therapy in CKD Patients.Nutrients · 2023Review
- Review
- Article
- Role of Dendritic Cell in Diabetic Nephropathy.International journal of molecular sciences · 2021Review
- Amplification of Salt-Sensitive Hypertension and Kidney Damage by Immune Mechanisms.American journal of hypertension · 2021Review
- SHROOM3, the gene associated with chronic kidney disease, affects the podocyte structure.Scientific reports · 2020Article
- Immune mechanisms of salt-sensitive hypertension and renal end-organ damage.Nature reviews. Nephrology · 2019Review
- Exosomal CCL2 from Tubular Epithelial Cells Is Critical for Albumin-Induced Tubulointerstitial Inflammation.Journal of the American Society of Nephrology : JASN · 2018Article
- IL-36 Signaling Facilitates Activation of the NLRP3 Inflammasome and IL-23/IL-17 Axis in Renal Inflammation and Fibrosis.Journal of the American Society of Nephrology : JASN · 2017Article
- Novel adaptive and innate immunity targets in hypertension.Pharmacological research · 2017Review
- The Tubulointerstitial Pathophysiology of Progressive Kidney Disease.Advances in chronic kidney disease · 2017Review
- Renal recruitment of B lymphocytes exacerbates tubulointerstitial fibrosis by promoting monocyte mobilization and infiltration after unilateral ureteral obstruction.The Journal of pathology · 2017Article
- Liraglutide Reduces Both Atherosclerosis and Kidney Inflammation in Moderately Uremic LDLr-/- Mice.PloS one · 2016Article
- Albuminuria Is an Appropriate Therapeutic Target in Patients with CKD: The Pro View.Clinical journal of the American Society of Nephrology : CJASN · 2015Review
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14 authors.
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No grant is acknowledged in the PubMed record.
Abstract
The role of dendritic cells (DC) that accumulate in the renal parenchyma of non-immune-mediated proteinuric nephropathies is not well understood. Under certain circumstances, DC capture immunologically ignored antigens, including self-antigens, and present them within MHC class I, initiating an autoimmune response. We studied whether DC could generate antigenic peptides from the self-protein albumin. Exposure of rat proximal tubular cells to autologous albumin resulted in its proteolytic cleavage to form an N-terminal 24-amino acid peptide (ALB1-24). This peptide was further processed by the DC proteasome into antigenic peptides that had binding motifs for MHC class I and were capable of activating syngeneic CD8+ T cells. In vivo, the rat five-sixths nephrectomy model allowed the localization and activation of renal DC. Accumulation of DC in the renal parenchyma peaked 1 wk after surgery and decreased at 4 wk, concomitant with their appearance in the renal draining lymph nodes. DC from renal lymph nodes, loaded with ALB1-24, activated syngeneic CD8+ T cells in primary culture. The response of CD8+ T cells of five-sixths nephrectomized rats was amplified with secondary stimulation. In contrast, DC from renal lymph nodes of five-sixths nephrectomized rats treated with the proteasomal inhibitor bortezomib lost their capacity to stimulate CD8+ T cells in primary and secondary cultures. These data suggest that albumin can be a source of potentially antigenic peptides upon renal injury and that renal DC play a role in processing self-proteins through a proteasome-dependent pathway.
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