ArticleFrontiers in immunology2026
Dual role of icaritin in attenuating allograft rejection and exerting antitumor effects in mice.
Article in Frontiers in immunology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
Background: Long-term immunosuppression following organ transplantation results in an elevated risk of malignancies in recipients, which constitutes a major factor limiting their long-term survival. Therefore, the development of immunosuppressant with anti-tumor efficacy holds critical significance. Icaritin (ICT), a clinically employed antitumor drug, enhances anti tumor immunity by reshaping the tumor immune microenvironment. Moreover, recent evidence highlights its immunomodulatory role in mitigating multiple autoimmune diseases. However, whether ICT can attenuate the allograft rejection remains poorly characterized. Methods: Fully major histocompatibility complex-mismatched heterotopic heart transplantation was conducted from BALB/c mice to C57BL/6J mice. The rejection of the allografts was assessed via H&E staining and immunohistochemistry. Single-cell RNA sequencing (scRNA-seq) and flow cytometry were carried out on recipient splenocytes. In vitro, isolated naïve CD4 Results: ICT markedly attenuated acute cardiac allograft rejection and enhanced graft survival. scRNA-seq and flow cytometric analyses revealed a significant reduction in the proportion of splenic Th1 cells in ICT-treated recipient mice. Conclusions: While exerting antitumor effects, ICT attenuates allograft rejection by targeting the CEBPB/PIM1 axis, thereby suppressing CD4
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