Innate lymphoid cells integrate sensing and plasticity to control fungal infections

Citation

Verified title: Innate lymphoid cells integrate sensing and plasticity to control fungal infections
Publication year: 2026
DOI: 10.1016/j.celrep.2026.117140
Metadata source: source PDF first page / DOI line (manual local verification)
Original local title: Innate lymphoid cells integrate sensing and plasticity to control fungal infections

Ingest Mode

Mode: focused manual crystallization mode
Meaning: this source page was manually reviewed for source text, model context, assay directness, and claim boundaries.
Durable synthesis status: selected source-specific claims were propagated into entity/topic/digest pages only where evidence strength and context labels are preserved.

Source Type

primary pulmonary fungal-infection ILC sensing and plasticity study
Evidence profile: fungal-cell-wall component sensing, Syk/p38 signaling, Aspergillus fumigatus lung infection, cytokine-driven ILC3 skewing, adoptive ILC transfer, Tec kinase perturbation, fungal burden, inflammation, and survival.
Knowledge note status: source-reviewed evidence note suitable for lung infection and ILC plasticity synthesis.

Evidence Profile

Overall confidence: high for the source-specific claim that pulmonary ILCs can sense fungal components and reshape antifungal immunity in mouse lung infection systems.
Evidence tags: #source/primary #species/mouse #tissue/lung #cell/ILC1 #cell/ILC2 #cell/ILC3 #assay/flow #assay/RNAseq #assay/in_vivo #assay/in_vitro #assay/KO #outcome/infection #outcome/inflammation #axis/ILC_lung_infection #axis/ILC_plasticity #status/focused_crystallization
Primary biological axis: fungal sensing -> Syk/p38 and Tec-linked signaling -> early ILC activation and cytokine-conditioned ILC3-skewed plasticity during antifungal response.

Why It Matters Here

This source adds direct pulmonary fungal-infection evidence to a wiki that previously emphasized viral, bacterial, asthma, and inflammatory injury contexts. It is especially useful because it connects sensing, signaling, adoptive ILC function, and ILC plasticity in one lung infection model.

Key Findings

Pulmonary ILCs responded to fungal components, with Syk/p38-dependent signaling implicated in activation.
Aspergillus fumigatus infection created an inflammatory cytokine environment that promoted ILC3-like skewing during the response.
In vitro cytokine combinations supported ILC2-to-ILC3 and ILC1-to-ILC3 phenotypic shifts under defined inflammatory conditions.
Adoptive ILC transfer altered lung infection outcomes in lymphocyte-deficient recipients, and Tec-deficient ILCs were linked to improved antifungal protection in the reported system.

Claim-Level Confidence

High confidence: this is direct mouse lung fungal-infection evidence for ILC sensing and response modulation.
Medium-high confidence: cytokine-driven ILC plasticity toward ILC3-like states is a relevant interpretation branch for pulmonary fungal inflammation.
Medium confidence: Tec signaling is a candidate therapeutic axis, but the evidence remains model-specific.
Low confidence: this source does not by itself establish human aspergillosis or asthma treatment relevance.

Methods and Context

Species/context: mouse pulmonary Aspergillus fumigatus infection and in vitro fungal/cytokine stimulation systems.
Assay directness: strong for lung infection and ILC activation/plasticity in the reported model.
Key modalities: fungal challenge, flow cytometry, adoptive transfer, genetic kinase perturbation, cytokine stimulation, fungal-burden and survival/inflammation readouts.
Best wiki use: fungal lung infection, ILC sensing, Syk/p38, Tec kinase, and ILC1/ILC2-to-ILC3-like plasticity.

Caveats

Keep the fungal-infection model distinct from allergic asthma and bacterial pneumonia.
ILC3-like skewing should be described as context- and assay-dependent unless lineage tracing proves durable conversion.
Tec-deficient transfer findings should stay within the adoptive-transfer and mouse infection context.

Contradiction and Supersession

Contradiction status: complements prior bacterial and viral infection branches by adding a fungal-specific sensing/plasticity axis.
Supersession status: new direct pulmonary infection branch, not a replacement for influenza, RSV, tuberculosis, or pneumococcal evidence.