High-Priority Manual Crystallization Batch 2

Why this audit happened

The user requested the second high-priority paper manual crystallization pass before creating new mechanism entity pages. Batch 2 focuses on human lung ILC subset baselines, COPD/smoke-associated plasticity, allergen or cytokine-induced ILC plasticity, and additional neutrophilic or steroid-resistant asthma framing.

Sources revisited

• 11 high-priority source pages were manually crystallized from extracted title, abstract, early results text, and current wiki context.
• The batch synthesis has been integrated into Lung ILC Core Evidence Synthesis.
• The entity hubs ILC2 and ILC3 were updated after batch 1 and batch 2 claims were consolidated.

Page families changed

• Source pages: 11 high-priority papers upgraded with mature Key Findings, Claim-Level Confidence, Methods and Context, Caveats, and contradiction framing.
• Digest pages: one new batch 2 digest created.
• Entity pages: ILC2 and ILC3 hubs updated to hold high-confidence claim anchors from both high-priority digests.
• Navigation pages: index, digest README, source README, project page, main topic page, and log updated.

Rule or interpretation changes

• Human lung baseline evidence is now separated from disease mechanism evidence.
• ILC2 plasticity is now split into memory-like allergic, COPD-associated ILC1-like, IL-17-producing ST2+ ILC2, and human nasal IL-17-producing branches.
• ILC3 steroid-resistant asthma evidence is separated into primary human airway association, mouse perturbation, and review-level therapeutic target framing.
• Source Claim-Level Confidence remains claim-centered and does not discuss file presence or extraction status.

Crystallized source pages

• Characterization and Quantification of Innate Lymphoid Cell Subsets in Human Lung
• Spatial and Temporal Mapping of Human Innate Lymphoid Cells Reveals Elements of Tissue Specificity
• Inflammatory triggers associated with exacerbations of COPD orchestrate plasticity of group 2 innate lymphoid cells in the lungs
• Cigarette smoke aggravates asthma by inducing memory-like type 3 innate lymphoid cells
• Innate Lymphoid Cells Are Required to Induce Airway Hyperreactivity in a Murine Neutrophilic Asthma Model
• Group 3 Innate Lymphoid Cells A Potential Therapeutic Target for Steroid Resistant Asthma
• Allergen-Experienced Group 2 Innate Lymphoid Cells Acquire Memory-like Properties and Enhance Allergic Lung Inflammation
• IL-17-producing ST2(+) group 2 innate lymphoid cells play a pathogenic role in lung inflammation
• IL-1beta, IL-23, and TGF-beta drive plasticity of human ILC2s towards IL-17-producing ILCs in nasal inflammation
• Group 2 innate lymphoid cells (ILC2) are regulated by stem cell factor during chronic asthmatic disease
• Innate immune crosstalk in asthmatic airways Innate lymphoid cells coordinate polarization of lung macrophages

Follow-up actions

• Consider a later focused COPD/smoke digest if those sources become a project priority.
• Consider mechanism entity pages later for IL-12/IL-18, IL-33/leukotrienes/Ahr, CD45RO memory-like ILC3, SCF/KIT, and ILC-macrophage crosstalk. The user explicitly deferred this step for now.

Reviewer-gate notes

• Verdict: no blocking accuracy issues detected in the batch-level claims after checking selected extracted source text and existing wiki context.
• Supported with caveat: human lung and sputum data are mostly association or ex vivo functional evidence; mouse perturbation evidence remains stronger for causal claims.
• Supported with caveat: nasal ILC2-to-IL-17 plasticity was preserved as human airway/nasal evidence, not lower-lung proof.
• Supported with caveat: the steroid-resistant asthma review was used for target-space framing and not as primary clinical efficacy evidence.