Group 3 innate lymphoid cells mediate early protective immunity against tuberculosis

Citation

Verified title: Group 3 innate lymphoid cells mediate early protective immunity against tuberculosis
Publication year: 2019
DOI: 10.1038/s41586-019-1276-2
Metadata source: crossref-doi (confidence: high)
Original local title: Group 3 innate lymphoid cells mediate early protective immunity against tuberculosis

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 human tuberculosis and mouse pulmonary infection study
Evidence profile: blood ILC profiling in human tuberculosis, treatment-associated restoration, mouse aerosol Mtb infection, lung ILC3 accumulation, ILC3-deficient phenotypes, and CXCL13/IL-17/IL-22-linked early granuloma logic.
Knowledge note status: source-reviewed evidence note suitable for pulmonary ILC3 infection-defense synthesis.

Evidence Profile

Overall confidence: high for a source-specific early protective role of ILC3s in the reported tuberculosis systems.
Evidence tags: #source/primary #species/human #species/mouse #tissue/lung #cell/ILC3 #cell/macrophage #assay/flow #assay/in_vivo #assay/KO #outcome/infection #outcome/inflammation #axis/ILC_lung_infection #status/focused_crystallization
Primary biological axis: Mtb-induced ILC3 accumulation, IL-17/IL-22-dependent CXCL13 induction, alveolar macrophage recruitment, and early granuloma formation.

Why It Matters Here

This paper broadens the ILC3 lung model beyond asthma by adding a direct pulmonary bacterial infection source. It is one of the strongest local sources for ILC3s as protective organizers of early lung immunity rather than only IL-17-associated pathology.

Key Findings

Human tuberculosis was associated with altered circulating ILC subsets, with ILC1s and ILC3s rebounding after treatment in paired samples.
Mouse aerosol Mtb infection induced rapid pulmonary ILC3 accumulation that coincided with alveolar macrophage accumulation.
ILC3-deficient mice showed impaired early alveolar macrophage accumulation, smaller early granulomas, and reduced Mtb control in the reported system.
IL-17 and IL-22 from ILC3s were implicated in induction of lung CXCL13 and early innate granuloma organization.

Claim-Level Confidence

High confidence: ILC3s support early protective pulmonary immunity to Mtb in the reported mouse model.
Medium-high confidence: human tuberculosis data support disease relevance through circulating ILC subset changes and treatment-associated restoration, but tissue causality is primarily mouse-based.
Low confidence: this source should not be generalized to all bacterial pneumonias or to late-stage tuberculosis immunopathology without matching evidence.

Methods and Context

Species/context: human tuberculosis blood profiling and mouse aerosol Mtb lung infection.
Assay directness: strong for mouse ILC3 functional requirement; supportive for human disease relevance.
Best wiki use: ILC3 infection defense, CXCL13/granuloma organization, and macrophage-linked lung immunity.

Caveats

The human and mouse evidence layers answer different questions; do not merge them into a single causal human lung claim.
The protective role is early and model-specific; late infection, pathology, and treatment contexts may differ.
Keep tuberculosis separate from viral infection and asthma branches.

Contradiction and Supersession

Contradiction status: balances ILC3 asthma/ARDS pathology sources by showing a protective infection-defense branch.
Supersession status: not superseded; it should be added to the representative pulmonary ILC3 source spine.