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Background: The tumor microenvironment (TME) is integral to tumor progression. However, its prognostic implications and underlying mechanisms in clear cell renal cell carcinoma (ccRCC) are not yet fully elucidated. This study aims to examine the prognostic significance of genes associated with immune-stromal scores and to explore their underlying mechanisms in ccRCC.

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Highly sensitized (HS) patients in need of kidney transplantation (KTx) typically spend a longer time waiting for compatible kidneys, are unlikely to receive an organ offer, and are at increased risk of antibody-mediated rejection (AMR). Desensitization using imlifidase, which is more rapid and removes total body immunoglobulin G (IgG) to a greater extent than other methods, enables transplantation to occur between HLA-incompatible (HLAi) donor-recipient pairs and allows patients to have greater access to KTx. However, when the project was launched there was limited data and clinical experience with desensitization in general and with imlifidase specifically.

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Polyomavirus BK (BKPyV)-associated nephropathy (BKPyV-nephropathy) remains a significant cause of premature kidney allograft failure. In the absence of effective antiviral treatments, current therapeutic approaches rely on immunosuppression (IS) reduction, possibly at the risk of inducing alloimmunity. Therefore, we sought to explore the long-term effects of a tailored viro-immunologic surveillance and treatment program for BKPyV on the development of alloimmunity and kidney graft outcome.

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The objective of this study was to examine the association between serum tacrolimus trough levels and the detection of BK viruria in kidney transplant recipients. We conducted a retrospective study and included kidney transplant recipients who underwent BK viruria screening during 2018-2021. Serum tacrolimus trough levels, urine BK viral load, and potential risk factors were collected.

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Engineered antigen-specific T regulatory cells suppress autoreactivity to the anti-glomerular basement membrane disease antigen.

Kidney Int

January 2025

Centre for Inflammatory Diseases, Department of Medicine, School of Clinical Sciences, Monash University, Clayton, Australia. Electronic address:

Anti-glomerular basement membrane (anti-GBM) disease is accompanied by insufficient antigen-specific T regulatory cells (Tregs) and clonally expanded antigen-specific T conventional cells (Tconvs). In particular, this applied to the immunodominant T cell auto- epitope of type IV collagen, α3(IV)NC1135-145 , presented by HLA-DR15. Here, we investigated whether Tregs engineered to express GBM-T cell receptors (TCR) specific for α3(IV)NC1135- 145 better suppress autoimmunity.

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