ArticleCancer immunology, immunotherapy : CII2026
Naringin promotes cancer immunity by inducing cross-presentation by antigen-presenting cells.
Article in Cancer immunology, immunotherapy : CII, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.