Donor–Recipient Non-HLA Variants, Mismatches and Renal Allograft Outcomes: Evolving Paradigms

Jethwani, Priyanka; Rao, Arundati; Bow, Laurine; Menon, Madhav C.

doi:10.3389/fimmu.2022.822353

Cited by 7 publications

(9 citation statements)

References 106 publications

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“…According to a previous study, Cldn8 overexpression leads to the downregulation of Cldn2 expression (36). The hyperexpression of Epb41L2, Prkcb, Shroom3 are implicated in adhesion damage (37)(38)(39). MBZ is a classic chemotherapeutic agent available for CE treatment (40).…”

Section: Discussionmentioning

confidence: 99%

The non-oral infection of larval Echinococcus granulosus induces immune and metabolic reprogramming in the colon of mice

Zhou

Luo²,

Gong³

et al. 2023

Front. Immunol.

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BackgroundThe intestinal tract serves as a critical regulator for nutrient absorption and overall health. However, its involvement in anti-parasitic infection and immunity has been largely neglected, especially when a parasite is not transmitted orally. The present study investigated the colonic histopathology and functional reprogramming in mice with intraperitoneal infection of the larval Echinococcus granulosus (E. granulosus).ResultsCompared with the control group, the E. granulosus–infected mice exhibited deteriorated secreted mucus, shortened length, decreased expression of tight junction proteins zonula occludens-1 (ZO-1), and occludin in the colon. Moreover, RNA sequencing was employed to characterize colonic gene expression after infection. In total, 3,019 differentially expressed genes (1,346 upregulated and 1,673 downregulated genes) were identified in the colon of infected mice. KEGG pathway and GO enrichment analysis revealed that differentially expressed genes involved in intestinal immune responses, infectious disease-associated pathways, metabolism, or focal adhesion were significantly enriched. Among these, 18 tight junction-relative genes, 44 immune response-associated genes, and 23 metabolic genes were annotated. Furthermore, mebendazole treatment could reverse the colonic histopathology induced by E. granulosus infection.ConclusionsIntraperitoneal infection with E. granulosus induced the pathological changes and functional reprogramming in the colon of mice, and mebendazole administration alleviated above alternations, highlighting the significance of the colon as a protective barrier against parasitic infection. The findings provide a novel perspective on host-parasite interplay and propose intestine as a possible target for treating parasitic diseases that are not transmitted orally.

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Section: Discussionmentioning

confidence: 99%

The non-oral infection of larval Echinococcus granulosus induces immune and metabolic reprogramming in the colon of mice

Zhou

Luo²,

Gong³

et al. 2023

Front. Immunol.

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“…There is increasing evidence that donor-recipient mismatches at non-HLA regions may also be responsible for alloimmunity leading to chronic rejection and allograft loss. These mechanisms are discussed in detail by Jethwani et al [ 36 ]. There are currently limited diagnostic and therapeutic options for the prevention or treatment of non-HLA antibody mediated rejection.…”

Section: Pre-transplant Measuresmentioning

confidence: 99%

Preventing Rejection of the Kidney Transplant

Malhotra,

Jethwani

2023

JCM

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With increasing knowledge of immunologic factors and with the advent of potent immunosuppressive agents, the last several decades have seen significantly improved kidney allograft survival. However, despite overall improved short to medium-term allograft survival, long-term allograft outcomes remain unsatisfactory. A large body of literature implicates acute and chronic rejection as independent risk factors for graft loss. In this article, we review measures taken at various stages in the kidney transplant process to minimize the risk of rejection. In the pre-transplant phase, it is imperative to minimize the risk of sensitization, aim for better HLA matching including eplet matching and use desensitization in carefully selected high-risk patients. The peri-transplant phase involves strategies to minimize cold ischemia times, individualize induction immunosuppression and make all efforts for better HLA matching. In the post-transplant phase, the focus should move towards individualizing maintenance immunosuppression and using innovative strategies to increase compliance. Acute rejection episodes are risk factors for significant graft injury and development of chronic rejection thus one should strive for early detection and aggressive treatment. Monitoring for DSA development, especially in high-risk populations, should be made part of transplant follow-up protocols. A host of new biomarkers are now commercially available, and these should be used for early detection of rejection, immunosuppression modulation, prevention of unnecessary biopsies and monitoring response to rejection treatment. There is a strong push needed for the development of new drugs, especially for the management of chronic or resistant rejections, to prolong graft survival. Prevention of rejection is key for the longevity of kidney allografts. This requires a multipronged approach and significant effort on the part of the recipients and transplant centers.

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“…Potential confounding factors influencing the association between genetic markers and renal rejection include different gene-expression-analysis technologies (microarray vs. RNAseq), obtaining extra biopsy cores for profiling, and variability in blood tacrolimus concentrations affecting transplant outcomes and AR risk [ 62 ]. One of the most critical genetic markers for renal rejection is the HLA mismatch, which refers to differences in human leukocyte antigen between the donor and recipient [ 63 , 64 ]. The HLA system plays a crucial role in presenting antigens to the immune system and is involved in the recognition and rejection of foreign tissues.…”

Section: Genetic Markersmentioning

confidence: 99%

Biomarkers for Kidney-Transplant Rejection: A Short Review Study

Sharaby,

Alksas,

Abou El-Ghar

et al. 2023

Biomedicines

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Kidney transplantation is the preferred treatment for end-stage renal failure, but the limited availability of donors and the risk of immune rejection pose significant challenges. Early detection of acute renal rejection is a critical step to increasing the lifespan of the transplanted kidney. Investigating the clinical, genetic, and histopathological markers correlated to acute renal rejection, as well as finding noninvasive markers for early detection, is urgently needed. It is also crucial to identify which markers are associated with different types of acute renal rejection to manage treatment effectively. This short review summarizes recent studies that investigated various markers, including genomics, histopathology, and clinical markers, to differentiate between different types of acute kidney rejection. Our review identifies the markers that can aid in the early detection of acute renal rejection, potentially leading to better treatment and prognosis for renal-transplant patients.

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Donor–Recipient Non-HLA Variants, Mismatches and Renal Allograft Outcomes: Evolving Paradigms

Cited by 7 publications

References 106 publications

The non-oral infection of larval Echinococcus granulosus induces immune and metabolic reprogramming in the colon of mice

The non-oral infection of larval Echinococcus granulosus induces immune and metabolic reprogramming in the colon of mice

Preventing Rejection of the Kidney Transplant

Biomarkers for Kidney-Transplant Rejection: A Short Review Study

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