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Lung ILC Disease Roles Companion

Scope

This page is a companion page to Lung ILC Core Evidence Synthesis, not a parallel digest competing with it.

Use the core evidence page as the main cross-subset synthesis. Use this companion when you want the same biology rearranged by disease context rather than by cell state.

Evidence tags

#tissue/lung #cell/ILC1 #cell/ILC2 #cell/ILC3 #digest/companion_page #disease/asthma #disease/infection #disease/ARDS

Disease-first map

flowchart TD
    accTitle: Pulmonary ILC Disease Roles Companion
    accDescr: Disease-first map showing how ILC2 and ILC3 branches map onto allergic asthma, viral injury and repair, bacterial defense, ARDS-like injury, and neutrophilic asthma.

    disease["Pulmonary disease context"] --> asthma2["Type 2 asthma"]
    disease --> virus["Viral injury / repair"]
    disease --> bacteria["Bacterial defense"]
    disease --> ards["ARDS-like injury"]
    disease --> asthma3["Neutrophilic / steroid-resistant asthma"]

    asthma2 --> ilc2a["ILC2: IL-5 / IL-13 / AHR"]
    virus --> ilc2b["ILC2: AHR, AREG, GM-CSF"]
    bacteria --> ilc3a["ILC3: IL-22"]
    ards --> ilc3b["ILC3-linked IL-17A"]
    asthma3 --> ilc3c["ILC3: IL-17A, SCF/KIT, steroid resistance"]

    classDef disease_class fill:#e8f3ff,stroke:#3b6ea8,stroke-width:2px,color:#17324d
    classDef branch_class fill:#eef7ed,stroke:#4d8a50,stroke-width:2px,color:#173d1d
    classDef cell_class fill:#fff4de,stroke:#b47a1f,stroke-width:2px,color:#4a3108

    class disease disease_class
    class asthma2,virus,bacteria,ards,asthma3 branch_class
    class ilc2a,ilc2b,ilc3a,ilc3b,ilc3c cell_class

Disease-oriented reading guide

Disease question Dominant ILC branch Best next page Representative anchors
Allergic or eosinophilic asthma ILC2 type 2 amplification ILC2 Roles In Pulmonary Disease Innate lymphoid cells mediate influenza-induced airway hyper-reactivity independently of adaptive immunity, Lung type 2 innate lymphoid cells express cysteinyl leukotriene receptor 1 which regulates TH2 cytokine production
Upstream drivers of type 2 or eosinophilic airway disease ILC2 alarmin, lipid, neuroimmune, stromal, and metabolic regulation ILC2 Functional Regulation Mechanisms Cysteinyl leukotriene E4 activates human group 2 innate lymphoid cells and enhances the effect of prostaglandin D2 and epithelial cytokines, The Role of the TL1A/DR3 Axis in the Activation of Group 2 Innate Lymphoid Cells in Subjects with Eosinophilic Asthma, Lipid-Droplet Formation Drives Pathogenic Group 2 Innate Lymphoid Cells in Airway Inflammation
Viral airway physiology versus repair ILC2 AHR, AREG, BATF, GM-CSF branches ILC2 Innate lymphoid cells promote lung-tissue homeostasis after infection with influenza virus, BATF promotes group 2 innate lymphoid cell-mediated lung tissue protection during acute respiratory virus infection
Bacterial defense and neonatal pulmonary niches ILC3 IL-22 and IGF1-supported developmental branch ILC3 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
ARDS-like injury or neutrophilic inflammation ILC3-linked IL-17A and neutrophil programs ILC3 Roles In Pulmonary Disease Innate Lymphoid Cells Are the Predominant Source of IL-17A during the Early Pathogenesis of Acute Respiratory Distress Syndrome, Group 3 innate lymphoid cells secret neutrophil chemoattractants and are insensitive to glucocorticoid via aberrant GR phosphorylation
Smoke-associated, neutrophilic, or steroid-resistant asthma ILC3 memory-like, SCF/KIT, glucocorticoid-insensitive, and obesity-associated IL-17 branches ILC3 Functional Regulation Mechanisms Cigarette smoke aggravates asthma by inducing memory-like type 3 innate lymphoid cells, Pulmonary fibroblast-derived stem cell factor promotes neutrophilic asthma by augmenting IL-17A production from ILC3s, Interleukin-17-producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity

Interpretation boundaries

  • Asthma should not be treated as one ILC disease. The wiki separates at least a type 2/eosinophilic ILC2-dominant branch and a neutrophilic/steroid-resistant ILC3-associated branch.
  • Viral lung disease should not be collapsed into one effect. Some ILC2 programs drive airway physiology, whereas others support tissue repair or macrophage-state remodeling.
  • Bacterial defense, neonatal development, ARDS-like injury, and smoke-associated asthma use different ILC outputs and should stay separated.
  • Human lung tissue, sputum, blood, BAL, nasal airway, and mouse perturbation evidence answer different questions and should remain labeled.

How This Companion Fits The Wiki

This page no longer serves as a second full synthesis layer parallel to the core digest. Instead:

  • Lung ILC Core Evidence Synthesis is the main cross-subset interpretation page.
  • ILC2 and ILC3 are the canonical cell hubs.
  • This page is the disease-first rearrangement for readers who think in pathology or endotypes rather than in cell-state architecture.

Representative Source Spine