Fungal / mucocutaneous barrier
Dectin-style fungal sensing and epithelial alarm promote IL-17 programs, neutrophil recruitment, antimicrobial peptides, and barrier repair.
Signals
Cells
Questions
Pitfalls
clinical pattern
IL-17 barrier recruitment, neutrophil support, mucocutaneous defense, and dysbiosis loops
Review layer
Last reviewed 2026-05-17
Systems teaching draft. Content is structured for education and graph expansion, with formal source tagging ready for the next review pass.
Provenance layer
Curated external IDs add pathway and protein context around Atlas content. They do not update the graph automatically and they are not patient-specific interpretation.
State signature
System effects
Primary mapped axes from existing Atlas data.
Tissue
Organ, barrier, stromal, vascular, or local niche behavior.
Inflammation
Inflammatory alarm, recruitment, mediator release, or tissue-damaging amplification.
Neuroimmune
Nerve, neuropeptide, autonomic, microglial, pain, itch, fatigue, or sickness-behavior coupling.
No direct axis cue is mapped for this node yet.
Pattern signature
Signals
01IL-17
IL-6
IL-1beta
TGF-beta
CXCL8/IL-8
Cells
02TH17 cells
neutrophils
dendritic cells
macrophages
Tissues
03gut
skin
mucosal lymphoid
lung
Restraint
04Tregs
IL-10
barrier restoration
microbiome resilience
controlled neutrophil resolution
Graph neighborhood
Context link: no causal arrow.
TH17 cells coordinate IL-17-rich mucocutaneous barrier defense and neutrophil recruitment
Context link: no causal arrow.
IL-17 is the signature barrier recruitment signal for fungal and extracellular defense contexts
Context link: no causal arrow.
Mucosal lymphoid tissues organize antigen sampling, TH17 instruction, IgA context, and barrier memory
Context link: no causal arrow.
Skin barrier disruption can recruit IL-17-neutrophil loops that are protective or inflammatory depending on context
Pattern logic
Assess barrier integrity, mucosal fungal pressure, dysbiosis, neutrophil recruitment, IL-17 amplification, and whether the same pathway is protective or tissue-injuring in context.
Pathogen-class context
Dectin-style fungal sensing and epithelial alarm promote IL-17 programs, neutrophil recruitment, antimicrobial peptides, and barrier repair.
Signals
Cells
Questions
Pitfalls
Protozoa are heterogeneous: intracellular protozoa often require TH1/macrophage activation, while tissue-invasive or eosinophil-linked contexts may recruit type 2 or granulomatous features.
Signals
Cells
Questions
Pitfalls
Large multicellular parasites favor epithelial alarmins, TH2/ILC2 tone, IgE, mast cells, eosinophils, mucus, smooth muscle activation, and repair programs.
Signals
Cells
Questions
Pitfalls