AI Article Synopsis
- Human cytomegalovirus (CMV) infection can cause kidney transplant issues, especially when paired with acute rejection, and this study looks at CMV-induced antibodies in that context.
- Researchers used mice to assess immunoglobulin G (IgG) and complement deposition in various types of CMV-infected kidney transplants, comparing B cell-deficient recipients and the effects of treatment with immune sera.
- Findings showed that kidney transplants with certain CMV profiles had higher IgG and complement deposition, leading to more significant tissue damage, suggesting that the body's immune response to CMV plays a role in kidney transplant rejection.
Article Abstract
Background: Human cytomegalovirus (CMV) infection is associated with renal allograft dysfunction and loss, particularly in combination with acute rejection. Emerging literature suggests that non-HLA antibodies may contribute to antibody-mediated rejection, but pathogen-induced antibodies have not been investigated in this context. This study examines the presence of CMV-induced antibodies in murine CMV (MCMV)-infected renal allografts during acute rejection.
Methods: Intragraft immunoglobulin G (IgG) and complement C3 immunostaining were compared among allogeneic MCMV D-/R-, D+/R-, and D+/R+ renal transplants. Intragraft antibody deposition was examined in B cell-deficient recipients treated with MCMV immune sera. Antibody binding and complement-dependent cytotoxicity (CDC) of D-/R- and D+/R+ sera against infected renal tubular epithelial cells (TECs) were measured in vitro. IgG immunostaining was performed in D+/R+ allografts and native kidneys and in D+/R- allografts treated with ganciclovir to inhibit viral replication.
Results: D+/R- and D+/R+ transplants had more abundant IgG and C3 deposition compared with D-/R- recipients. Greater IgG deposition was associated with more severe allograft injury in B cell-deficient recipients treated with MCMV immune sera compared with nonimmune sera. D+/R+ sera induced greater CDC of infected TECs compared with D-/R- sera. Native kidneys had lower IgG deposition compared with allografts, despite similar organ viral loads. Ganciclovir-treated allografts had reduced IgG deposition compared with untreated allografts.
Conclusions: In this murine model, complement-fixing antibodies can deposit into MCMV-infected renal allografts, are associated with allograft damage, and can induce CDC of MCMV-infected renal TECs. The allogeneic response and viral replication may also contribute to intragraft antibody deposition.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8128940 | PMC |
| http://dx.doi.org/10.1097/TP.0000000000003548 | DOI Listing |
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