Natural Tr1-like cells do not form a functionally stable memory response to allergens, and this instability may limit efforts to re-establish tolerance by expanding Tr1.

Simultaneous cytokine signaling results in unexpected transcription factor changes that fuel a cellular response divergent from the sum of each cytokine alone.

In a Ugandan birth cohort, early childhood infection-exposure, notably to malaria, helminths, and diarrhoea, is associated with lower prevalence of atopy and allergy-related diseases in later childhood.

The genome of a tiny tomato pest reveals mechanisms that underlie metazoan genome reduction.

Using unique data from five longitudinal UK birth cohorts, four distinct subsets of genetic variants were identified as differentially associated across wheezing phenotypes from infancy to adolescence with little evidence of genetic associations spanning across different phenotypes.

Results in mice suggest that vitamin D reduces the symptoms of asthma by controlling an immune response that leads to inflammation of the airways.

Overgrowth of the yeast Pichia kudriavzevii within the neonatal gut microbiota increases allergic airway disease severity later in life and may be inhibited by short-chain fatty acids.

Lung interstitial macrophages are strategically positioned underneath the bronchial airway epithelium and enriched at airway bifurcations for immunosurveillance of the conducting airway lumen and the initiation of adaptive immune responses.

Asthma risk among schoolchildren increases depending on area of residence in early life, from rural to town to city, and this risk increases further with other known risk factors.

HMGB1 drives the development of paucigranulocytic asthma in RAGE deficient mice.