Scholarlink

<p>Successful immune checkpoint inhibitor (ICI) treatment of cancer requires adequate infiltration of cytotoxic CD8+T lymphocytes (CTLs) in tumors. Previous studies have identified the compound naringin, which increases CTL infiltration and rescues ICI efficacy in CTL-lacking tumors, and cancer CTL priming has been shown to rely on antigen cross-presentation (XPT). Therefore, the present study aimed to examine the effect of naringin on XPT by various human and murine antigen-presenting cells (APCs). The results indicated that naringin increases XPT by XPT-competent APCs, including murine bone marrow (BM) dendritic cells, peritoneal macrophages (MΦs), and human monocyte-derived dendritic cells (HMDCs). However, XPT was not observed with BM- or human monocyte-derived MΦs with or without naringin. Naringin reduced the activity of lysosomes, suppressing the degradation of internalized antigens, thereby increasing antigen cytosolic escape and MHC class I molecule-presenting antigens. In addition, human lymph node (LN) sinus MΦs were transcriptomically more similar to XPT-competent HMDCs than other LN MΦ groups. Taken together, these data suggest that naringin promotes XPT by XPT-competent APCs, which may explain why naringin was found to promote cancer immunity in our previous studies. This finding highlights the potential for developing cancer immunotherapies that induce XPT, offering a promising strategy to enhance antitumor immune responses.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Naringin promotes cancer immunity by inducing cross-presentation by antigen-presenting cells

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年7月26日

查看全文
  • Cheng Pan,
  • Yukio Fujiwara,
  • Daiki Yoshii,
  • Jiahao Pan,
  • Takuya Shiota,
  • Yuko Miyasato,
  • Yuka Mizue,
  • Yoshihiko Hirohashi,
  • Yoshihiro Komohara

摘要

Successful immune checkpoint inhibitor (ICI) treatment of cancer requires adequate infiltration of cytotoxic CD8+T lymphocytes (CTLs) in tumors. Previous studies have identified the compound naringin, which increases CTL infiltration and rescues ICI efficacy in CTL-lacking tumors, and cancer CTL priming has been shown to rely on antigen cross-presentation (XPT). Therefore, the present study aimed to examine the effect of naringin on XPT by various human and murine antigen-presenting cells (APCs). The results indicated that naringin increases XPT by XPT-competent APCs, including murine bone marrow (BM) dendritic cells, peritoneal macrophages (MΦs), and human monocyte-derived dendritic cells (HMDCs). However, XPT was not observed with BM- or human monocyte-derived MΦs with or without naringin. Naringin reduced the activity of lysosomes, suppressing the degradation of internalized antigens, thereby increasing antigen cytosolic escape and MHC class I molecule-presenting antigens. In addition, human lymph node (LN) sinus MΦs were transcriptomically more similar to XPT-competent HMDCs than other LN MΦ groups. Taken together, these data suggest that naringin promotes XPT by XPT-competent APCs, which may explain why naringin was found to promote cancer immunity in our previous studies. This finding highlights the potential for developing cancer immunotherapies that induce XPT, offering a promising strategy to enhance antitumor immune responses.