Focused Manual Crystallization Batch 3

Why this audit happened

The user requested formal ingest of 17 papers: 10 selected older provisional bulk-ingest papers, 6 newly added RAW PDFs, and one specified processed SCF/KIT ILC3 paper. This audit records that the batch was handled as focused manual crystallization mode, not provisional bulk ingest.

Sources revisited

• Innate lymphoid cells contribute to allergic airway disease exacerbation by obesity
• ILC2-driven innate immune checkpoint mechanism antagonizes NK cell antimetastatic function in the lung
• Blocking the HIF-1alpha glycolysis axis inhibits allergic airway inflammation by reducing ILC2 metabolism and function
• Eosinophils promote effector functions of lung group 2 innate lymphoid cells in allergic airway inflammation in mice
• c-Kit-positive ILC2s exhibit an ILC3-like signature that may contribute to IL-17-mediated pathologies
• Dopamine inhibits group 2 innate lymphoid cell-driven allergic lung inflammation by dampening mitochondrial activity
• Neuromedin-U Mediates Rapid Activation of Airway Group 2 Innate Lymphoid Cells in Mild Asthma
• mTORC1 signaling in group 2 innate lymphoid cells coordinates neuro-immune crosstalk in allergic lung inflammation
• PD-1 pathway regulates ILC2 metabolism and PD-1 agonist treatment ameliorates airway hyperreactivity
• Mechanics-activated fibroblasts promote pulmonary group 2 innate lymphoid cell plasticity propelling silicosis progression
• Differentiation of type 1 ILCs from a common progenitor to all helper-like innate lymphoid cell lineages
• Tissue residency of innate lymphoid cells in lymphoid and nonlymphoid organs
• The neuropeptide NMU amplifies ILC2-driven allergic lung inflammation
• Regulation of type 2 innate lymphoid cell-dependent airway hyperreactivity by butyrate
• Tissue signals imprint ILC2 identity with anticipatory function
• Pulmonary IL-33 orchestrates innate immune cells to mediate respiratory syncytial virus-evoked airway hyperreactivity and eosinophilia
• Pulmonary fibroblast-derived stem cell factor promotes neutrophilic asthma by augmenting IL-17A production from ILC3s

Page families changed

• Source pages: 17 pages were upgraded or reaffirmed as focused manual crystallization source notes.
• Digest pages: integrated into Lung ILC Core Evidence Synthesis.
• Entity pages: updated ILC2 and ILC3 with batch 3 claim additions.
• Topic pages: updated ILC2 and ILC3 regulation/disease pages with batch 3 mechanisms.
• Project, index, and log pages: updated for navigation and traceability.

Rule or interpretation changes

• The 10 selected older papers are no longer merely provisional bulk-ingest notes; their source pages now carry focused manual crystallization mode.
• The 6 newly added RAW PDFs were first registered, extracted, moved to RAW/processed/, and then promoted into the same focused batch.
• Durable synthesis from this batch should preserve disease model, tissue compartment, species, and assay boundaries.

Follow-up actions

• Consider a dedicated ILC2 neuroimmune-metabolic regulation in asthma digest.
• Consider a focused ILC3/stromal niche digest if SCF/KIT, IGF1, HB-EGF, and PDGF-D sources become a major project branch.
• Before manuscript use, re-check individual figure panels and methods for each source-specific claim.