Abstract
IL-23/IL-17 axis is an important regulator in various inflammatory diseases. However, the role of IL-23 in allergic airway inflammation is not well understood. In this study, we show that in an allergen-induced asthma model, mice with transgenic overexpression of IL-23R exhibited increased airway infiltration of eosinophils and Th2 cytokine production, whereas those deficient in IL-23 displayed reduced airway inflammation. In vitro, IL-23-IL-23R signaling promoted GATA-3 expression and enhanced Th2 cytokine expression. Conversely, in the absence of this signal, Th2 cell differentiation was partially inhibited. Therefore, IL-23 signaling may regulate allergic asthma through modulation of Th2 cell differentiation.
Publication types
-
Research Support, N.I.H., Extramural
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adaptive Immunity / immunology
-
Allergens / pharmacology
-
Animals
-
Asthma / immunology*
-
Asthma / physiopathology*
-
Cell Differentiation / genetics
-
Cell Differentiation / immunology
-
Cell Polarity / genetics
-
Cell Polarity / immunology
-
Chemotaxis, Leukocyte / immunology
-
Disease Models, Animal
-
GATA3 Transcription Factor / genetics
-
GATA3 Transcription Factor / metabolism
-
Gene Expression Regulation / genetics
-
Gene Expression Regulation / immunology
-
Humans
-
Interleukin-23 / metabolism*
-
Mice
-
Mice, Inbred C57BL
-
Mice, Knockout
-
Mice, Transgenic
-
Receptors, Interleukin / genetics
-
Respiratory System / immunology*
-
Respiratory System / physiopathology*
-
Signal Transduction / genetics
-
Signal Transduction / immunology
-
Th2 Cells / immunology*
-
Th2 Cells / metabolism
-
Up-Regulation / immunology
Substances
-
Allergens
-
GATA3 Transcription Factor
-
Gata3 protein, mouse
-
Interleukin-23
-
Receptors, Interleukin
-
interleukin-23 receptor, mouse