The Stat6VT mouse model of atopic dermatitis (AD) is induced by T-cell-specific expression of a constitutively active form of the protein signal transducer and activator of transcription 6 (STAT6).
Glyteer, Soybean Tar, Impairs IL-4/Stat6 Signaling in Murine Bone Marrow-Derived Dendritic Cells: The Basis of Its Therapeutic Effect on Atopic Dermatitis.
Moreover, there was a significant association between genotype and allele frequencies of the STAT6 (G2946A) polymorphism in the non-AD (P < 0.05) and AD (P < 0.01) groups.
The authors describe that it is the combination of changes in the skin barrier proteins filaggrin and Tmem79, together with Th2 cytokine signaling in the constitutively active Stat6 transgene, that drives the immune-pathomechanism in AD.
We used data from the Han Chinese in Beijing genome panel of International HapMap Project and the Taiwan Children Health Study cohort to investigate the association of STAT6 genetic variants and childhood AD risks.
Our study adds to the current knowledge of genetic susceptibility by demonstrating for the first time an interactive effect between SNPs in IL13 (rs20541) and STAT6 (rs1059513) on the occurrence of eczema in two independent samples.
Taken together, results of this investigation reveal that IL-4 signals through the Jak1, 2/Stat6 pathway in keratinocytes to stimulate CCL26 expression and this may provide an explanation for the pathogenesis of AD.
Recent studies have shown that polymorphisms in the genes for interleukin (IL)-4, the IL-4 receptor, IL-13, and signal transducer and activator 6 (STAT6) may contribute to susceptibility of AD.
We undertook an association study between these variants of the STAT6 gene and allergic diseases, including atopic dermatitis, bronchial asthma, and food-related anaphylaxis in a Japanese population.
IL-18 contributes to the spontaneous development of atopic dermatitis-like inflammatory skin lesion independently of IgE/stat6 under specific pathogen-free conditions.