Antigen-Presentation Competence in Gynecologic Cancers: Mechanisms, Evidence and Translational Priorities.
- 1School of Chinese Medicine, Hubei University of Chinese Medicine, Wuhan 430065, China.
- 2School of Basic Medical Sciences, Hubei University of Chinese Medicine, Wuhan 430065, China.
- 3The First Clinical Medical School, Hubei University of Chinese Medicine, Wuhan 430065, China.
Abstract
Immune-checkpoint biomarkers in gynecologic cancers primarily estimate antigenic potential or characterize an inhibited immune response. However, they do not establish whether malignant cells are visible to antigen-specific lymphocytes. We define antigen-presentation competence as the capacity of the tumor-immune ecosystem to generate antigenic peptides, display them through functional human leukocyte antigen molecules, prime cognate T cells through professional antigen-presenting cells, and permit recognition of malignant cells by effector lymphocytes. Recurrent defects have been reported at each step in cervical, endometrial, and ovarian cancers, but the evidence is not equally mature across these diseases. Cervical studies emphasize human papillomavirus-associated immune selection and antigen-processing machinery abnormalities; endometrial cancer provides relatively direct treatment-linked evidence for major histocompatibility complex class I and interferon-pathway defects; and ovarian cancer offers direct immunopeptidomic and multiregion evidence that antigen availability, presentation, and immune recognition can diverge. Taken together, the literature makes antigen-presentation competence a testable functional framework. It does not yet justify a biomarker or clinical score. Prospective work will need spatial and longitudinal measurements of tumor presentation, dendritic-cell priming, and T-cell recognition. A key test is whether these measurements improve prediction beyond mismatch repair, polymerase epsilon, programmed death-ligand 1, and tumor mutational burden.
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BibTeX
@article{xu2026antigenpresentation,
title = {{Antigen-Presentation Competence in Gynecologic Cancers: Mechanisms, Evidence and Translational Priorities.}},
author = {Zihao Xu and Yifan Liu and Jun Xu and Mengxin Xiong},
journal = {Cells},
year = {2026},
month = oct,
doi = {10.3390/cells15191809},
url = {https://europepmc.org/article/MED/42882506},
note = {CC BY},
}
RIS
TY - JOUR
TI - Antigen-Presentation Competence in Gynecologic Cancers: Mechanisms, Evidence and Translational Priorities.
AU - Zihao Xu
AU - Yifan Liu
AU - Jun Xu
AU - Mengxin Xiong
PY - 2026
DA - 2026/10/03
JO - Cells
DO - 10.3390/cells15191809
UR - https://europepmc.org/article/MED/42882506
AB - Immune-checkpoint biomarkers in gynecologic cancers primarily estimate antigenic potential or characterize an inhibited immune response. However, they do not establish whether malignant cells are visible to antigen-specific lymphocytes. We define antigen-presentation competence as the capacity of the tumor-immune ecosystem to generate antigenic peptides, display them through functional human leukocyte antigen molecules, prime cognate T cells through professional antigen-presenting cells, and permit recognition of malignant cells by effector lymphocytes. Recurrent defects have been reported at each step in cervical, endometrial, and ovarian cancers, but the evidence is not equally mature across these diseases. Cervical studies emphasize human papillomavirus-associated immune selection and antigen-processing machinery abnormalities; endometrial cancer provides relatively direct treatment-linked evidence for major histocompatibility complex class I and interferon-pathway defects; and ovarian cancer offers direct immunopeptidomic and multiregion evidence that antigen availability, presentation, and immune recognition can diverge. Taken together, the literature makes antigen-presentation competence a testable functional framework. It does not yet justify a biomarker or clinical score. Prospective work will need spatial and longitudinal measurements of tumor presentation, dendritic-cell priming, and T-cell recognition. A key test is whether these measurements improve prediction beyond mismatch repair, polymerase epsilon, programmed death-ligand 1, and tumor mutational burden.
SN - 2073-4409
ER -