TY - JOUR
T1 - IL-33 links tissue cells, dendritic cells and Th2 cell development in a mouse model of asthma
AU - Eiwegger, Thomas
AU - Akdis, Cezmi A.
PY - 2011/6
Y1 - 2011/6
N2 - IL-33 is becoming a central molecule in allergic asthma that addresses various cascades of innate and adaptive immune responses that lead to inflammation in the lung. Its effects are exerted via its heterodimeric receptor that consists of ST2 and the ubiquitously expressed IL-1 receptor accessory protein (ILRAcP). IL-33 integrates both innate and adaptive immunity in a unique fashion via basophils, mast cells, eosinophils, innate lymphoid cells, NK and NKT cells, nuocytes, Th2 lymphocytes and a CD34pos precursor cell population. These actions of IL-33 seem to be particularly strong and dominant in models with mucosal inflammation. A study in this issue of the European Journal of Immunology demonstrates that IL-33 acts, in an ST2-dependent manner, as a maturation factor for BM-derived DCs via up-regulation of CD80, CD40 and OX40L. This process is accompanied by the release of pro-inflammatory cytokines, such as IL-6, IL-1β, TNF-α and TARC/CCL17. IL-33-pre-treated DCs were significantly more potent for the generation of allergen-specific Th2-type cells with IL-5 and IL-13 production. Intratracheal administration of OVA-pulsed DCs with IL-33 significantly enhances eosinophil numbers and mucous secretion. In conclusion, IL-33 affects both the development of allergic sensitization and the development of lung inflammation in allergic asthma.
AB - IL-33 is becoming a central molecule in allergic asthma that addresses various cascades of innate and adaptive immune responses that lead to inflammation in the lung. Its effects are exerted via its heterodimeric receptor that consists of ST2 and the ubiquitously expressed IL-1 receptor accessory protein (ILRAcP). IL-33 integrates both innate and adaptive immunity in a unique fashion via basophils, mast cells, eosinophils, innate lymphoid cells, NK and NKT cells, nuocytes, Th2 lymphocytes and a CD34pos precursor cell population. These actions of IL-33 seem to be particularly strong and dominant in models with mucosal inflammation. A study in this issue of the European Journal of Immunology demonstrates that IL-33 acts, in an ST2-dependent manner, as a maturation factor for BM-derived DCs via up-regulation of CD80, CD40 and OX40L. This process is accompanied by the release of pro-inflammatory cytokines, such as IL-6, IL-1β, TNF-α and TARC/CCL17. IL-33-pre-treated DCs were significantly more potent for the generation of allergen-specific Th2-type cells with IL-5 and IL-13 production. Intratracheal administration of OVA-pulsed DCs with IL-33 significantly enhances eosinophil numbers and mucous secretion. In conclusion, IL-33 affects both the development of allergic sensitization and the development of lung inflammation in allergic asthma.
KW - Animal models
KW - Asthma
KW - Cytokines
KW - DCs
KW - Interleukin-1 Receptor-Like 1 Protein
KW - Interleukin-33
KW - Humans
KW - Th2 Cells/immunology
KW - Interleukins/immunology
KW - Mice, Knockout
KW - Animals
KW - Asthma/immunology
KW - Respiratory Hypersensitivity/immunology
KW - Receptors, Interleukin/genetics
KW - Myeloid Progenitor Cells/immunology
KW - Dendritic Cells/immunology
KW - Mice
KW - Disease Models, Animal
UR - http://www.scopus.com/inward/record.url?scp=79957537407&partnerID=8YFLogxK
U2 - 10.1002/eji.201141668
DO - 10.1002/eji.201141668
M3 - Editorial
C2 - 21618506
AN - SCOPUS:79957537407
SN - 0014-2980
VL - 41
SP - 1535
EP - 1538
JO - European Journal of Immunology
JF - European Journal of Immunology
IS - 6
ER -