ILC3

Scope

This entity page defines group 3 innate lymphoid cells (ILC3s) as they are used in the ILC-in-lung wiki. It is the canonical ILC3 hub for this wiki.

Use this page when the question is "what is the current source-aware ILC3 model in lung biology?" Then move to disease or regulation topics when you need a narrower branch.

Evidence tags

#entity/cell_type #cell/ILC3 #tissue/lung #topic/pulmonary_disease #topic/regulation #status/working

At a glance

Lens	Current take
Canonical role	Lung ILC3s are IL-22/IL-17-capable innate lymphocytes whose pulmonary roles split into host-defense/developmental and inflammatory-disease branches.
Strongest pulmonary branches	Pneumococcal IL-22 defense, neonatal IGF1-supported niche biology, ARDS-like IL-17 injury, smoke-associated asthma, neutrophilic asthma, and steroid-resistant asthma.
Strongest regulatory layers	Stromal licensing, cytokine-driven IL-17 programs, glucocorticoid resistance, tissue identity control, and boundary-state taxonomy.
Main caution	ILC3 is not shorthand for either protection or pathology; interpretation depends on mediator, compartment, model, and whether the data are human, mouse, or ex vivo.

How to use this page

• Start with Integrated working model and Review map for orientation.
• Use Major biological branches for disease or developmental context.
• Use Regulatory architecture for mechanism and identity questions.
• Use Interpretation guardrails before promoting ILC3 claims into broader synthesis or translational framing.

Confidence snapshot

• High confidence: human lung tissue contains identifiable ILC3 subsets, including NCR+ and NCR- ILC3 compartments, with inducible IL-17A, IL-22, and GM-CSF potential after stimulation (Characterization and Quantification of Innate Lymphoid Cell Subsets in Human Lung).
• High confidence: lung ILC3 biology splits into protective/developmental and inflammatory branches, including IL-22 during Streptococcus pneumoniae infection, fibroblast-derived IGF1 support of neonatal pulmonary ILC3s, and IL-17A-associated ARDS-like injury (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).
• High confidence: smoking asthma is associated with increased sputum NCR- ILC3s and blood CD45RO+ memory-like ILC3s, aligning with neutrophil and M1 macrophage signals rather than eosinophils (Cigarette smoke aggravates asthma by inducing memory-like type 3 innate lymphoid cells).
• High confidence: ILC3s can participate in neutrophilic or steroid-resistant asthma biology through neutrophil chemoattractants, glucocorticoid-insensitive programs, and fibroblast-derived SCF/KIT-driven IL-17A augmentation, but the strength of evidence varies by source and model (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).
• Medium-high confidence: ILCs are required for AHR in a murine low-dose LPS neutrophilic asthma model, and lung ILC3s increase in that model, but the causal transfer claim should be worded as broad ILC requirement rather than ILC3-only causality (Innate Lymphoid Cells Are Required to Induce Airway Hyperreactivity in a Murine Neutrophilic Asthma Model).
• Medium confidence: ILC3-related IL-17/neutrophilic pathways are a coherent candidate therapeutic mechanism space for non-eosinophilic or steroid-resistant asthma, but review-level therapeutic framing needs primary intervention evidence before being treated as stronger evidence (Group 3 Innate Lymphoid Cells A Potential Therapeutic Target for Steroid Resistant Asthma).
• Medium-high confidence: obesity-associated airway hyperreactivity can proceed through an NLRP3-IL-1beta-IL-17-producing innate-lymphoid branch that is distinct from canonical eosinophilic asthma framing (Interleukin-17-producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity).
• Medium confidence: extrapulmonary IL-23 biology includes an ILC3-intrinsic CTLA-4 checkpoint-restraint branch, which is useful for mechanism framing but should remain explicitly gut-labeled until matched pulmonary evidence appears (CTLA-4-expressing ILC3s restrain interleukin-23-mediated inflammation).

• Medium-high confidence: ILC3 identity and cytokine sustainment are also shaped by extrapulmonary but mechanistically important pathways including AHR and WASH-driven identity maintenance, vitamin D-mediated IL-23 restraint, a CD71-iron nutrient axis, and IRE1alpha/XBP1-dependent cytokine sustainment (AHR drives the development of gut ILC22 cells and postnatal lymphoid tissues via pathways dependent on and independent of Notch; WASH maintains NKp46+ ILC3 cells by promoting AHR expression; Vitamin D downregulates the IL-23 receptor pathway in human mucosal group 3 innate lymphoid cells; Nutrition impact on ILC3 maintenance and function centers on a cell-intrinsic CD71-iron axis; The IRE1alpha/XBP1 pathway sustains cytokine responses of group 3 innate lymphoid cells in inflammatory bowel disease).

• High confidence: in tuberculosis, ILC3s have an early protective pulmonary branch in which mouse lung ILC3-derived IL-17/IL-22 supports CXCL13 induction, alveolar macrophage accumulation, early granuloma formation, and Mtb control; human blood ILC changes support disease relevance but not direct human tissue causality (Group 3 innate lymphoid cells mediate early protective immunity against tuberculosis).

• Medium-high confidence: human severe-asthma sputum data add a direct airway ILC3/neutrophilia branch and an ILC2/ILC3-like boundary state that should be separated from bona fide pulmonary ILC3 claims unless marker and compartment labels are preserved (A population of c-kit+ IL-17A+ ILC2s in sputum from individuals with severe asthma supports ILC2 to ILC3 trans-differentiation).
• Medium confidence: several ILC3 regulatory mechanisms in the current source set are gut or mucosal rather than lung-specific, but they sharpen interpretation of ILC3 state control: IL-17D/CD93 supports IL-22-producing ILC3 function, reciprocal transcription-factor networks shape tissue-resident ILC3 identity, NPM1 supports mitochondrial OXPHOS and IL-22 activity, and PDGF-D drives species- and receptor-dependent outputs through mouse PDGFRbeta or human NKp44 contexts (Interleukin-17D regulates group 3 innate lymphoid cell function through its receptor CD93; Reciprocal transcription factor networks govern tissue-resident ILC3 subset function and identity; Nucleophosmin 1 promotes mucosal immunity by supporting mitochondrial oxidative phosphorylation and ILC3 activity; Divergent ILC3 responses to PDGF-D control mucosal immunity).
• Medium-high confidence for extrapulmonary adaptive-immunity context: gut and mucosal ILC3s can regulate CD4 T-cell tolerance, Treg maintenance/selection, and regulatory B-cell differentiation through MHCII, IL-2, alphaV integrin, CD40L, BAFF, IL-15, and CTLA-4-linked pathways; these mechanisms should remain gut/tonsil/blood-labeled until matched pulmonary data are added (ILC Regulation Of Adaptive Immunity).
• Medium confidence: extrapulmonary ILC3 antigen-presentation outcomes can diverge by context, including gut tolerance, CNS neuroinflammation, and colon-cancer immunotherapy response; RORgammat-positive DC lineage data add an attribution boundary for Treg-related mechanisms (Antigen-presenting innate lymphoid cells orchestrate neuroinflammation; Dysregulation of ILC3s unleashes progression and immunotherapy resistance in colon cancer; RORgammat+ dendritic cells are a distinct lymphoid-derived lineage).
• Medium confidence: gut/mucosal ILC3 regulation includes RANKL/RANK restraint, BMAL1/circadian timing, FFAR2 metabolite sensing, VIP neuroimmune circuits, trained defense states, and HB-EGF tissue-protection output; these sharpen regulatory interpretation but remain extrapulmonary context for this lung wiki.
• Medium confidence: gut/mucosal ILC3 context includes ZBTB46-linked protective identity, RORgammat-associated circadian epigenetic plasticity control, enteric GABA-Igfbp7 homeostatic support, RANK-linked tuft-cell/anthelmintic crosstalk, and human mucosal ILC3/ILC1-like diversity; these are useful taxonomy and mechanism guardrails rather than direct lung claims.
• Medium-high confidence: BACH2-PPARgamma and LINGO4-linked pathways add gut ILC3 metabolic/homeostatic guardrails, while pulmonary fungal infection and streptomycin dysbiosis sources add direct lung type 3 infection/inflammation branches (BACH2 controls ILC3 function via PPARgamma-dependent mitochondrial metabolism; LINGO4 coordinates ILC3-intrinsic IL-22 production and microbiota-mediated ILC3 homeostasis; Innate lymphoid cells integrate sensing and plasticity to control fungal infections; Microbial dysbiosis sculpts a systemic ILC3/IL-17 axis governing lung inflammatory responses and central hematopoiesis).
• Medium-high confidence: human severe-asthma blood and induced-sputum data support a sex- and compartment-aware ILC3 interpretation, with increased blood ILC3/IL-17+/IL-22+ signals in females with severe asthma and increased sputum RORgammat+ ILC3s in severe asthma; these are clinical association data rather than causal ILC3 proof (Severe asthma is characterized by a sex-specific ILC landscape and aberrant airway profile that is suppressed by anti-IL-5/5Ralpha biologics).

Integrated working model

The lung ILC3 model in this wiki has three durable branches. The first is a human pulmonary baseline branch: human lung tissue contains identifiable NCR+ and NCR- ILC3-like compartments with inducible IL-17A, IL-22, and GM-CSF potential. The second is a protective/developmental branch, where ILC3s contribute IL-22-mediated antibacterial defense and IGF1-supported neonatal pulmonary niche biology. The third is an inflammatory pathology branch, where IL-17A-, neutrophil-, smoke-, stromal-, and glucocorticoid-resistance-associated programs become central in ARDS-like injury and severe asthma endotypes.

The practical rule is to avoid treating ILC3 as automatically protective or pathogenic. The relevant biological unit is an ILC3-associated output in a defined lung context: IL-22 defense, IL-17A/neutrophilic inflammation, developmental niche support, or a noncanonical mediator branch such as acetylcholine. Around those branches sits an identity-support layer, mostly defined in gut or mucosal sources, in which AHR, WASH, vitamin D, nutrient handling, and ER-stress programs shape how durable or inflammatory an ILC3 state can become.

Review map

flowchart TD
    accTitle: ILC3 Review Map
    accDescr: Review-style map of the main pulmonary ILC3 branches in this wiki.

    baseline["Human lung baseline"] --> defense["IL-22 defense / development"]
    baseline --> injury["IL-17 injury / neutrophilic asthma"]
    baseline --> identity["Identity / boundary states"]
    defense --> regulators["Regulatory architecture"]
    injury --> regulators
    identity --> regulators
    regulators --> guardrails["Interpretation guardrails"]

    classDef entry fill:#e8f3ff,stroke:#3b6ea8,stroke-width:2px,color:#17324d
    classDef branch fill:#eef7ed,stroke:#4d8a50,stroke-width:2px,color:#173d1d
    classDef mech fill:#fff4de,stroke:#b47a1f,stroke-width:2px,color:#4a3108
    classDef caution fill:#f6eefc,stroke:#7a55a3,stroke-width:2px,color:#2d1645

    class baseline entry
    class defense,injury,identity branch
    class regulators mech
    class guardrails caution

Major biological branches

Human lung baseline

• Human lung baseline: ILC3s are detectable in human lung as CD117+ pulmonary ILCs subdivided into NCR+ and NCR- compartments by NKp44, and pulmonary ILCs can show IL-17A, IL-22, and GM-CSF potential after stimulation (Characterization and Quantification of Innate Lymphoid Cell Subsets in Human Lung).

Protective and developmental branches

• Protective/developmental branch: ILC3s can produce IL-22 during Streptococcus pneumoniae infection, while alveolar fibroblast-derived IGF1 supports neonatal pulmonary ILC3 development and antibacterial defense (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).

• Tuberculosis infection defense: ILC3s accumulate rapidly in mouse lungs after aerosolized Mtb infection and support early protective granuloma organization through IL-17/IL-22-CXCL13-linked logic; this is a protective infection branch, not an asthma pathology branch (Group 3 innate lymphoid cells mediate early protective immunity against tuberculosis).

Injury, neutrophilic asthma, and steroid resistance

• Injury/neutrophilic branch: pulmonary ILC3s can be a major early IL-17A source in ARDS-like injury, and ILCs are required for AHR in a low-dose LPS neutrophilic asthma model in which lung ILC3s and IL-1beta/IL-17A/IL-22 increase (Innate Lymphoid Cells Are the Predominant Source of IL-17A during the Early Pathogenesis of Acute Respiratory Distress Syndrome; Innate Lymphoid Cells Are Required to Induce Airway Hyperreactivity in a Murine Neutrophilic Asthma Model).
• Obesity-associated inflammatory branch: high-fat-diet airway hyperreactivity in mice can proceed through macrophage-derived IL-1beta, NLRP3, and CCR6-positive IL-17-producing innate lymphoid cells, supporting a nonatopic metabolic-airway branch rather than a simple eosinophilic-asthma extension (Interleukin-17-producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity).

• Smoke/steroid-resistant branch: smoking asthma is associated with sputum NCR- ILC3s and blood CD45RO+ memory-like ILC3s; human non-eosinophilic asthma ILC3s can secrete neutrophil chemoattractants and resist glucocorticoid suppression in vitro; review-level SRA literature frames ILC3-related IL-17/neutrophilic pathways as a candidate therapeutic mechanism space (Cigarette smoke aggravates asthma by inducing memory-like type 3 innate lymphoid cells; Group 3 innate lymphoid cells secret neutrophil chemoattractants and are insensitive to glucocorticoid via aberrant GR phosphorylation; Group 3 Innate Lymphoid Cells A Potential Therapeutic Target for Steroid Resistant Asthma).

• Human severe-asthma sputum data indicate that ILC3s are increased in neutrophilic airway inflammation, while mixed granulocytic inflammation contains c-kit+ IL-17A+ intermediate ILC2s; this source strengthens the need to separate bona fide ILC3s from ILC2-derived or ILC2/ILC3-like boundary states (A population of c-kit+ IL-17A+ ILC2s in sputum from individuals with severe asthma supports ILC2 to ILC3 trans-differentiation).

• Fungal infection branch: pulmonary ILCs can sense fungal components and influence Aspergillus lung infection outcomes, with inflammatory cytokines supporting ILC3-like skewing in the reported mouse system (Innate lymphoid cells integrate sensing and plasticity to control fungal infections).
• Gut-lung type 3 branch: streptomycin-induced dysbiosis can prime lung ILC3/Th17 inflammation in mouse hypersensitivity pneumonitis, linking microbiome state, IL-23, bile-acid metabolites, mTORC1, and central hematopoietic remodeling (Microbial dysbiosis sculpts a systemic ILC3/IL-17 axis governing lung inflammatory responses and central hematopoiesis).

Stromal and noncanonical mediator branches

• Stromal and noncanonical mediator branch: pulmonary fibroblast-derived SCF/KIT augments ILC3 IL-17A and neutrophilic asthma-like inflammation, while ILC3-derived acetylcholine promotes protease-driven allergic lung pathology in a separate mediator branch (Pulmonary fibroblast-derived stem cell factor promotes neutrophilic asthma by augmenting IL-17A production from ILC3s; ILC3-derived acetylcholine promotes protease-driven allergic lung pathology).
• Human airway crosstalk: induced-sputum asthma data associate ILC1/ILC3s with M1-like macrophage polarization and ILC2s with M2-like polarization, helping separate eosinophilic and noneosinophilic asthma branches (Innate immune crosstalk in asthmatic airways Innate lymphoid cells coordinate polarization of lung macrophages).

Regulatory architecture

Adaptive-immunity regulation

• Gut ILC3 MHCII sources support CD4 T-cell restraint and commensal-specific T-cell selection rather than simple T-cell priming (Innate lymphoid cells regulate CD4+ T-cell responses to intestinal commensal bacteria; Group 3 innate lymphoid cells mediate intestinal selection of commensal bacteria-specific CD4+ T cells).
• Intestinal ILC3s can support or select Tregs through IL-2 and antigen-presentation-linked mechanisms, while human tonsil/blood ILC3s can provide CD40L/BAFF/IL-15-linked help for regulatory B-cell differentiation (Innate lymphoid cells support regulatory T cells in the intestine through interleukin-2; ILC3s select microbiota-specific regulatory T cells to establish tolerance in the gut; Human CD40 ligand-expressing type 3 innate lymphoid cells induce IL-10-producing immature transitional regulatory B cells).
• These are strong adaptive-immunity mechanisms for ILC3 biology, but they are not yet direct lung ILC3 claims in this wiki.

SCF/KIT stromal licensing

• High confidence: pulmonary fibroblast-derived SCF/KIT augments ILC3 IL-17A and neutrophilic asthma-like inflammation, making stromal ILC3 licensing a core branch of the ILC3 lung model (Pulmonary fibroblast-derived stem cell factor promotes neutrophilic asthma by augmenting IL-17A production from ILC3s).
• Medium-high confidence: obesity-exacerbated allergic airway disease can involve both lung ILC2 and ILC3 responses in mouse models, but this should stay separate from lean type 2 asthma and human obesity-asthma claims (Innate lymphoid cells contribute to allergic airway disease exacerbation by obesity).

Effector-program and steroid-response layer

• High confidence: neutrophil-chemoattractant production, glucocorticoid insensitivity, and smoke-associated inflammatory conditioning are central to the current pulmonary ILC3 disease model (Group 3 innate lymphoid cells secret neutrophil chemoattractants and are insensitive to glucocorticoid via aberrant GR phosphorylation; Cigarette smoke aggravates asthma by inducing memory-like type 3 innate lymphoid cells).
• High confidence: a macrophage-derived IL-1beta and NLRP3 axis can license IL-17-producing innate lymphoid cells in obesity-associated airway hyperreactivity, adding a metabolic-inflammatory upstream layer to the pulmonary ILC3 model (Interleukin-17-producing innate lymphoid cells and the NLRP3 inflammasome facilitate obesity-associated airway hyperreactivity).

Restraint and counter-regulation

• Medium confidence: ILC3 biology also includes an ILC3-intrinsic CTLA-4 checkpoint branch that restrains IL-23-mediated inflammation in the gut; this is currently best used as conserved mechanism context rather than direct pulmonary evidence (CTLA-4-expressing ILC3s restrain interleukin-23-mediated inflammation).

• Medium-high confidence: human mucosal ILC3s also contain a vitamin D-linked restraint branch that downregulates IL-23-pathway responsiveness, which is useful as translational mechanism context but should remain gut-labeled until matched pulmonary evidence exists (Vitamin D downregulates the IL-23 receptor pathway in human mucosal group 3 innate lymphoid cells).

• Medium confidence: gut-labeled ILC3 mechanism sources add IL-17D/CD93 support of IL-22 output, NPM1-p65-TFAM support of mitochondrial OXPHOS, and PDGF-D receptor-context divergence; these are useful regulatory analogies but should not be promoted to lung causality without pulmonary data (Interleukin-17D regulates group 3 innate lymphoid cell function through its receptor CD93; Nucleophosmin 1 promotes mucosal immunity by supporting mitochondrial oxidative phosphorylation and ILC3 activity; Divergent ILC3 responses to PDGF-D control mucosal immunity).

Identity, nutrient, and stress regulation

• Medium-high confidence: AHR is a foundational ILC3 or ILC22 identity regulator, and WASH-Arid1a signaling helps maintain an NKp46-positive ILC3 branch by promoting AHR expression in gut-focused mechanistic sources (AHR drives the development of gut ILC22 cells and postnatal lymphoid tissues via pathways dependent on and independent of Notch; WASH maintains NKp46+ ILC3 cells by promoting AHR expression).

• Medium-high confidence: nutritional and stress-response pathways are integral to ILC3 state control; a CD71-iron axis supports metabolic fitness and host defense, while IRE1alpha/XBP1 sustains IL-23 or IL-1beta-responsive cytokine output in intestinal inflammation models (Nutrition impact on ILC3 maintenance and function centers on a cell-intrinsic CD71-iron axis; The IRE1alpha/XBP1 pathway sustains cytokine responses of group 3 innate lymphoid cells in inflammatory bowel disease).

• Medium-high confidence: reciprocal transcription-factor networks govern tissue-resident ILC3 subset function and identity, supporting conservative interpretation of ILC3 heterogeneity and plasticity rather than a single fixed IL-17/IL-22 cell model (Reciprocal transcription factor networks govern tissue-resident ILC3 subset function and identity).

• Medium confidence: gut/mucosal mechanism sources add RANKL/RANK, BMAL1/circadian timing, FFAR2, VIP/VPAC receptor context, trained ILC3 states, and HB-EGF as additional state-control or tissue-protection branches; these should be cited as extrapulmonary mechanism context unless pulmonary evidence is added.

Taxonomy and boundary states

• Medium-high confidence: helper-like ILC lineage and tissue-residency sources support conservative taxonomy for lung ILC3 interpretation: helper-like ILCs are developmentally distinct from conventional NK cells, and tissue ILCs can be resident sentinel populations (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).
• Medium-high confidence: IL-17-producing ILC-like cells require careful classification because c-Kit+ ILC2s can acquire ILC3-like IL-17-producing features, while SCF/KIT can also regulate bona fide pulmonary ILC3 IL-17A in neutrophilic asthma-like inflammation (c-Kit-positive ILC2s exhibit an ILC3-like signature that may contribute to IL-17-mediated pathologies; Pulmonary fibroblast-derived stem cell factor promotes neutrophilic asthma by augmenting IL-17A production from ILC3s).

Claim-level confidence boundaries

• High confidence is used for ILC3 claims supported by direct lung, airway, or pulmonary disease evidence linking ILC3 identity to IL-22, IL-17A, GM-CSF, neutrophil-associated inflammation, or developmental niche activity.
• Medium-high confidence is used when a mechanism is supported in lung-relevant models but still needs clearer human causality, compartment mapping, or pathway hierarchy.
• Medium confidence is used for therapeutic framing and broad endotype claims when the biology is coherent but primary intervention evidence remains limited.

Interpretation guardrails

ILC3s should be modeled as tissue-niche-responsive IL-22/IL-17-capable innate lymphocytes whose lung roles split into defense/development, acute injury, and neutrophilic or steroid-resistant airway disease branches. Protective IL-22 and pathogenic IL-17/neutrophil-associated programs can coexist in the literature; source interpretation depends on disease model, tissue compartment, cytokine program, and whether evidence is human association, ex vivo function, mouse perturbation, or review-level synthesis.

Contradiction and supersession

• IL-22-associated protection and IL-17-associated pathology can coexist in the ILC3 literature; interpretation depends on cytokine, disease model, timing, and tissue compartment.
• Human sputum, blood, BAL, and lung tissue should not be treated as interchangeable ILC3 compartments.
• ILC3 smoke/steroid-resistant asthma claims should distinguish primary human association, in vitro glucocorticoid resistance, mouse perturbation, and review-level therapeutic framing.
• IL-17-producing ST2+ ILC2s should not be collapsed into bona fide ILC3s without marker and lineage context.

Open questions

• Which ILC3 IL-17 pathways are conserved across ARDS, neutrophilic asthma, smoke-associated asthma, and infection?
• Are memory-like ILC3 states durable in human lung disease, or mostly model-specific?
• Which stromal niche signals, especially IGF1 and SCF/KIT, are shared between development and adult inflammatory lung disease?
• How should ILC3-derived acetylcholine be integrated with canonical IL-17/IL-22 disease models?

Reading routes

• For disease-first reading, go next to ILC3 roles in pulmonary disease.
• For mechanism-first reading, go next to ILC3 functional regulation mechanisms.

• For adaptive-immunity crosstalk, go next to ILC Regulation Of Adaptive Immunity.

• For cross-subset synthesis, go next to Lung ILC Core Evidence Synthesis.

Related pages

• ILC3 roles in pulmonary disease
• ILC3 functional regulation mechanisms

• ILC Regulation Of Adaptive Immunity

• Lung ILC Disease Roles Companion

• Lung ILC Core Evidence Synthesis
• Reference coverage notes

Future Expansion Directions

This short appendix highlights future literature directions rather than part of the current evidence summary. Literature that would most strengthen this entity page includes:

• Human lung, BAL, sputum, and scRNA-seq studies that harmonize ILC3 subset markers across asthma, COPD, ARDS, pneumonia, and lung cancer.
• Primary intervention studies separating ILC3 IL-17, neutrophil chemoattractants, SCF/KIT, and glucocorticoid-resistance mechanisms in steroid-resistant asthma.
• Spatial datasets linking fibroblast, epithelial, macrophage, and ILC3 neighborhoods in diseased lung.