High-Priority Manual Crystallization Batch 1

Why this audit happened

The user requested high-priority paper manual crystallization after the source pages were corrected to use biological claim confidence rather than file-processing confidence. This batch promotes a focused set of direct lung/airway ILC papers from provisional automated notes into mature source notes and a reusable digest.

Sources revisited

• 13 high-priority source pages were manually crystallized from extracted title, abstract, early results text, and current wiki context.
• The batch prioritizes direct lung or airway disease relevance, direct support for current topic/entity pages, and mechanistic importance for ILC2 or ILC3 function.
• The batch synthesis has been integrated into Lung ILC Core Evidence Synthesis.

Page families changed

• Source pages: 13 high-priority papers upgraded with mature Key Findings, Claim-Level Confidence, Methods and Context, Caveats, and contradiction framing.
• Digest pages: one crystallized batch digest added.
• Navigation pages: index, digest README, project hub, source README, and log updated.

Rule or interpretation changes

• First-pass mature source notes should preserve source-specific disease context and avoid universal ILC claims.
• Viral ILC2 biology is now explicitly split into pathogenic AHR, reparative amphiregulin/BATF, IL-1beta braking, and gammaherpesvirus-conditioned macrophage imprinting branches.
• ILC3 biology is now explicitly split into IL-22 bacterial defense, IGF1 neonatal development, IL-17A ARDS-like pathology, acetylcholine-associated protease allergy, and SCF/KIT neutrophilic asthma branches.

Crystallized source pages

• Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity
• Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus
• Lung type 2 innate lymphoid cells express cysteinyl leukotriene receptor 1 which regulates TH2 cytokine production
• Activation of Type 3 innate lymphoid cells and interleukin 22 secretion in the lungs during Streptococcus pneumoniae infection
• Insulin-like Growth Factor 1 Supports a Pulmonary Niche that Promotes Type 3 Innate Lymphoid Cell Development in Newborn Lungs
• Innate Lymphoid Cells Are the Predominant Source of IL-17A during the Early Pathogenesis of Acute Respiratory Distress Syndrome
• Kinetics of the accumulation of group 2 innate lymphoid cells in IL-33-induced and IL-25-induced murine models of asthma a potential role for the chemokine CXCL16
• ILC3-derived acetylcholine promotes protease-driven allergic lung pathology
• IL-1beta prevents ILC2 expansion, type 2 cytokine secretion, and mucus metaplasia in response to early-life rhinovirus infection in mice
• BATF promotes group 2 innate lymphoid cell-mediated lung tissue protection during acute respiratory virus infection
• Dampening type 2 properties of group 2 innate lymphoid cells by a gammaherpesvirus infection reprograms alveolar macrophages
• Group 3 innate lymphoid cells secret neutrophil chemoattractants and are insensitive to glucocorticoid via aberrant GR phosphorylation
• Pulmonary fibroblast-derived stem cell factor promotes neutrophilic asthma by augmenting IL-17A production from ILC3s

Follow-up actions

• Manually inspect full figures/methods for the 13 batch-1 papers before manuscript-level wording.
• Next source-note batch should focus on human lung ILC subset papers, COPD/smoke-associated ILC plasticity, and additional steroid-resistant asthma sources.
• Consider entity pages for IL33, IL13, amphiregulin, GM-CSF, IL22, IL17A, SCF/KIT, and BATF.

Reviewer-gate notes

• Verdict: no blocking accuracy issues detected in the batch-level claims after checking the selected extracted source text against the revised source pages and digest.
• Supported with caveat: human relevance claims were kept weaker than mouse perturbation claims when the source evidence was mouse-dominant or peripheral-blood-dominant.
• Supported with caveat: the 2011 influenza AHR paper is described as ILC2-like/natural-helper-cell biology because it predates current ILC2 terminology.
• Supported with caveat: imatinib in the SCF/KIT source is framed as experimental pathway inhibition, not as a clinical recommendation.
• Residual limitation: OCR artifacts and incomplete PDF extraction remain in some source text; full PDF figure/method review is still required before manuscript-level wording.