ArticleKidney international reports2025
The Effects of Clazakizumab on Peripheral Blood and Kidney Transcriptomes in Patients With Late Antibody-Mediated Rejection.
Article in Kidney international reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
1 citing paper in PubMed.
- Clazakizumab: A Therapeutic Approach for Patients With Late Antibody-Mediated Rejection.Kidney international reports · 2025Article
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10 authors.
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Abstract
Introduction: There are no licensed treatments for antibody-mediated rejection (AMR), a major cause of late kidney allograft loss. Clazakizumab (CLZ), an interleukin (IL)-6-neutralizing antibody, showed potential efficacy in a phase 2 trial in late AMR, with a reduction in donor-specific antibodies (DSAs) and kidney molecular microscope diagnostic system (MMDx) AMR score, but the underpinning mechanisms are unclear. Methods: Using peripheral blood transcriptomics, we identified a decrease in IL-6-associated "JAK-STAT signaling" pathway genes with CLZ, and a reduction in gene modules that enriched for T follicular helper cell and activated platelet signatures, cells that contribute to DSA generation and inflammatory responses to DSA respectively. However, responses were variable, and some patients showed a rebound in the expression of inflammatory signatures with long-term CLZ treatment, indicating variability in the efficacy of IL-6 antagonism. One peripheral blood gene module significantly correlated with kidney MMDx AMR score and enriched for monocyte signature genes, as well as "Fc gamma receptor-mediated phagocytosis" and "leukocyte transendothelial migration" gene sets, suggesting that cells activated by DSAs can be detected in peripheral blood. In the kidney, CLZ-treatment was associated with a significant reduction in a damaged tubule gene signature and preservation of podocyte signatures. We also found a kidney plasma cell gene-rich module that positively correlated with circulating DSAs; however, this was not significantly downregulated by CLZ. Conclusion: Overall, our results provide mechanistic insights into the effects and limitations, of IL-6 neutralization in humans in the context of AMR.
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