ArticleBMC immunology2017
Renal allograft rejection, lymphocyte infiltration, and de novo donor-specific antibodies in a novel model of non-adherence to immunosuppressive therapy.
Article in BMC immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 12 citations in OpenAlex.
- Article
- Extra centrosomes induce PIDD1-mediated inflammation and immunosurveillance.The EMBO journal · 2023Article
- B-cell activating factor BAFF as a novel alert marker for the immunological risk stratification after kidney transplantation.Immunologic research · 2021Article
- Structural Valve Deterioration Is Linked to Increased Immune Infiltrate and Chemokine Expression.Journal of cardiovascular translational research · 2021Article
- BAFF signaling drives interstitial transformation of mouse renal tubular epithelial cells in a Pin1-dependent manner.In vitro cellular & developmental biology. Animal · 2021Article
- Disruption of Tfh:B Cell Interactions Prevents Antibody-Mediated Rejection in a Kidney Transplant Model in Rats: Impact of Calcineurin Inhibitor Dose.Frontiers in immunology · 2021Article
- B Cell Activating Factor (BAFF) Is Required for the Development of Intra-Renal Tertiary Lymphoid Organs in Experimental Kidney Transplantation in Rats.International journal of molecular sciences · 2020Article
- Regulatory CD8 T cells that recognize Qa-1 expressed by CD4 T-helper cells inhibit rejection of heart allografts.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- IL-6 and IL-8 secreted by tumour cells impair the function of NK cells via the STAT3 pathway in oesophageal squamous cell carcinoma.Journal of experimental & clinical cancer research : CR · 2019Article
- Psychosocial Assessment of Candidates for Transplantation (PACT) Score Identifies High Risk Patients in Pediatric Renal Transplantation.Frontiers in pediatrics · 2019Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundNon-adherence has been associated with reduced graft survival. The aim of this study was to investigate the immunological mechanisms underlying chronic renal allograft rejection using a model of non-adherence to immunosuppressive therapy. We used a MHC (major histocompatibility complex) -mismatched rat model of renal transplantation (Brown Norway to Lewis), in which rats received daily oral cyclosporine A. In analogy to non-adherence to therapy, one group received cyclosporine A on alternating days only. Rejection was histologically graded according to the Banff classification. We quantified fibrosis by trichrome staining and intra-graft infiltration of T cells, B cells, and monocytes/macrophages by immunohistochemistry. The distribution of B lymphocytes was assessed using immunofluorescence microscopy. Intra-graft chemokine, chemokine receptor, BAFF (B cell activating factor belonging to the TNF family), and immunoglobulin G transcription levels were analysed by RT-PCR. Finally, we evaluated donor-specific antibodies (DSA) and complement-dependent cytotoxicity using flow cytometry.
resultsAfter 28 days, cellular rejection occurred during non-adherence in 5/6 animals, mixed with humoral rejection in 3/6 animals. After non-adherence, the number of T lymphocytes were elevated compared to daily immunosuppression. Monocyte numbers declined over time. Accordingly, lymphocyte chemokine transcription was significantly increased in the graft, as was the transcription of BAFF, BAFF receptor, and Immunoglobulin G. Donor specific antibodies were elevated in non-adherence, but did not induce complement-dependent cytotoxicity.
conclusionCellular and humoral rejection, lymphocyte infiltration, and de novo DSA are induced in this model of non-adherence.
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