Loading
Life sciences · Journal article
Frontiers in Immunology · September 28, 2026
No summary has been generated for this record yet. What follows is drawn from its source metadata only.
Journal article.
No findings were extractable from the material analysed.
Safety was not reported in the material analysed. Check the source before drawing any conclusion about harm.
The source did not state who this applies to in practice.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
This record has not been graded across any dimension yet. Treat the label above as provisional and read the source.
What is missing. This record has no bottom line, key findings, reported figures, evidence dimensions. That is a gap in the analysis, not a judgement about the study.
Triple-negative breast cancer (TNBC) is an aggressive and clinically challenging breast cancer subtype defined by the absence of estrogen receptor, progesterone receptor, and HER2 expression. Because these classical therapeutic targets are lacking, chemotherapy remains a central systemic treatment; however, TNBC is frequently associated with early recurrence, distant metastasis, immune escape, and therapeutic resistance. Growing evidence shows that these malignant features are strongly shaped by the tumor microenvironment (TME), a complex network of tumor cells, extracellular matrix, stromal cells, immune cells, vascular structures, cytokines, chemokines, and signaling mediators. Compared with hormone receptor-positive breast cancer, TNBC often displays stronger immune infiltration and higher immune-checkpoint activity, suggesting an immune-inflamed phenotype in many cases. Nevertheless, immune-cell presence does not always produce effective antitumor immunity because TNBC can develop PD-L1 upregulation, alternative checkpoint activation, antigen-presentation loss, T-cell exhaustion, macrophage polarization, regulatory T-cell expansion, myeloid-derived suppressor cell recruitment, stromal immune exclusion, hypoxia, metabolic stress, epigenetic regulation, and exosome-mediated immune suppression. This review summarizes TME-driven immune evasion in TNBC, emphasizing molecular heterogeneity, hot and cold immune phenotypes, immunosuppressive cellular networks, PD-1/PD-L1 signaling, stromal barriers, metastatic immune escape, advances in clinical immunotherapy, adverse effects, and emerging TME-directed strategies. Understanding these mechanisms may support rational combination therapies, biomarker-guided patient selection, and individualized immunotherapeutic approaches for TNBC.