Loading
Life sciences · Journal article
Advanced Science · September 30, 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.
Immune checkpoint inhibitors (ICIs) targeting CTLA-4 and PD-1 have transformed cancer therapy, yet their immune-related adverse events (irAEs) in various tissues, including the brain, remain poorly defined. ICI perturbs hippocampal-dependent memory function by derailing neuro-immune homeostasis and compromising synaptic integrity. However, the cellular and molecular mechanisms by which ICI alters regional interactions are not well understood. Using bulk RNA-sequencing and MERFISH spatial transcriptomics in a syngeneic murine melanoma model, we show that ICI treatment remodels hippocampal gene expression and cellular organization. While tumor burden itself altered brain physiology, ICI distinctly modified the abundance and transcriptional states of neurons, microglia, astrocytes, oligodendrocytes, and T cells, with coordinated induction of inflammatory, synaptic, and immune-response programs. Complementary analysis of human postmortem brain samples confirmed microglial activation as a key hallmark of ICI-treated brains, highlighting the translational relevance of our findings. Finally, using a conditional deletion model, we show that T cells are indispensable for ICI-driven microglial activation. Altogether, our results identify a T cell-microglia crosstalk axis as a driving mechanism of the pathophysiology of irAEs in the brain and provide a high-resolution spatial model for better understanding neuroinflammatory responses during ICI-induced unleashing of anti-tumor immunity.