House dust mite-driven neutrophilic airway inflammation in mice with TNFAIP3-deficient myeloid cells is IL-17-independent.
Heleen VromanTridib DasIngrid M BergenJennifer A C van HulstFatemeh AhmadiGeert van LooErik LubbertsRudi W HendriksMirjam KoolPublished in: Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology (2018)
These findings show that neutrophilic airway inflammation induced by activated TNFAIP3/A20-deficient myeloid cells can develop in the absence of IL-17RA-signalling. Neutrophilic inflammation is likely maintained by similar quantities of pro-inflammatory cytokines IL-1β and IL-6 that can, independently of IL-17-signalling, induce the expression of neutrophil chemo-attractants.
Keyphrases
- induced apoptosis
- cell cycle arrest
- rheumatoid arthritis
- dendritic cells
- bone marrow
- poor prognosis
- type diabetes
- endoplasmic reticulum stress
- signaling pathway
- cell death
- adipose tissue
- heavy metals
- insulin resistance
- wild type
- climate change
- drinking water
- long non coding rna
- combination therapy
- polycyclic aromatic hydrocarbons