# Hygiene Hypothesis

Specific microbial exposures can shape immune regulation and prevent some eczema; a generalized hygiene-to-allergy-and-autoimmunity causal chain is not established.

Overall Γ follows the registered complete human incidence SC3, with SC1 at Β and exposure-specific immune/clinical SC2 at Ε. Positive eczema trials and mechanistic recipient experiments are retained without claiming generalized protection from asthma or autoimmunity. Neither a universal biomarker cap nor a negative-trial veto is imposed on the narrow clinical successes; the broad conjunction has not crossed its own causal boundary.

Strain, dose, early versus later timing, maternal versus infant administration, delivery mode, genotype and disease endpoint map genuine boundaries. Post-hoc cesarean findings and genotype interactions are not prospectively validated rescue scopes. A human atopy/eczema outcome is not a clinical autoimmune incidence endpoint.