Dysregulation of ILC3s unleashes progression and immunotherapy resistance in colon cancer

Citation

Verified title: Dysregulation of ILC3s unleashes progression and immunotherapy resistance in colon cancer
Publication year: 2021
DOI: 10.1016/j.cell.2021.07.029
Metadata source: crossref-doi (confidence: high)
Original local title: Dysregulation of ILC3s unleashes progression and immunotherapy resistance in colon cancer

Ingest Mode

Mode: focused manual crystallization mode
Meaning: this source page has been manually reviewed for the adaptive-immunity follow-up question, including model system, tissue compartment, immune-cell target, assay directness, and claim-level boundaries.
Required boundary: reusable claims should preserve species, tissue, disease model, and whether evidence is primary perturbation, human association, ex vivo function, lineage taxonomy, or review-level synthesis.

Source Type

primary colon cancer ILC3-MHCII-immunotherapy study - Evidence profile: colorectal cancer, ILC3 dysregulation, ILC3-T-cell imbalance, ILC3-specific MHCII, microbiota-dependent type 1 immunity, anti-PD-1 resistance, and human-mouse transfer context. - Knowledge note status: source-reviewed evidence note for gut tumor ILC3-adaptive-immunity context.

Evidence Profile

Overall confidence: high for source-specific colon cancer evidence that ILC3 MHCII supports microbiota-linked type 1 immunity and immunotherapy responsiveness. - Evidence tags: #source/primary #species/mouse #species/human #tissue/gut #disease/cancer #cell/ILC3 #cell/T_cell #assay/in_vivo #assay/flow #outcome/immunotherapy #outcome/inflammation #axis/adaptive_immunity #axis/ILC_regulation #status/focused_crystallization - Primary biological axis: ILC3-T-cell dialogue through MHCII shapes microbiota-dependent type 1 antitumor immunity and anti-PD-1 responsiveness in colorectal cancer context.

Why It Matters Here

This source adds an adaptive-immunity and immunotherapy branch to ILC3 biology, while remaining explicitly colon cancer rather than lung cancer evidence.

Key Findings

Colorectal cancer was associated with altered ILC3 frequency, plasticity, and imbalance with T cells.
ILC3-T-cell dialogue through MHCII supported microbiota that induced type 1 immunity in intestine and tumor microenvironment.
ILC3-specific MHCII loss promoted invasive colorectal cancer and anti-PD-1 resistance in the reported mouse context.
Human dysregulated intestinal ILC3/microbiota transfer data supported translational relevance.

Claim-Level Confidence

High confidence: ILC3 MHCII is important for the reported colon cancer immunotherapy axis.
Medium-high confidence: ILC3-adaptive-immunity crosstalk can affect tumor immunity and immunotherapy response in gut cancer.
Low confidence: this should not be used as direct lung cancer evidence.

Methods and Context

Species/context: mouse colorectal cancer and human microbiota/ILC3 association-transfer context.
Compartment: gut tumor microenvironment.
Assay directness: strong for colon cancer context; indirect for lung.
Best wiki use: tumor/immunotherapy adaptive-immunity branch with tissue boundary.

Caveats

Keep colon cancer context explicit.
Do not generalize anti-PD-1 implications to lung cancer without matched evidence.
Separate microbiota-mediated type 1 immunity from direct T-cell priming.

Contradiction and Supersession

Contradiction status: extends ILC3 MHCII biology from tolerance to antitumor type 1 immunity.
Supersession status: not superseded.