Patients with AD may experience immune imbalance, increased levels of mast cells, immunoglobulin (Ig) E and pro-inflammatory factors (Cyclooxygenase, COX-2 and inducible NO synthase, iNOS).
In addition, we report a statistically non-significant change of the CD4+/CD8+ ratio, a dramatic decrease of three gene markers (PIAS1, RORA and SH2B1) as well as a panel of differential expression of cytokines in AD dogs in comparison to the healthy controls.
By examining the skin homogenate, we found that sclareol inhibited the AD-like severity likely through suppressions of both NF-kB translocation and phosphorylation of the MAP kinase pathway.
A T cell-intrinsic increase of gp130 expression upon Ets1 deficiency promotes the gp130-mediated IL-6 signaling pathway, thereby leading to the development of severe AD-like symptoms.
Patients with AD may experience immune imbalance, increased levels of mast cells, immunoglobulin (Ig) E and pro-inflammatory factors (Cyclooxygenase, COX-2 and inducible NO synthase, iNOS).
In pediatric AD blood, T helper (Th) type 2 (CCL13, CCL22) and Th17 (peptidase inhibitor-3/elafin) markers were increased, together with markers of tissue remodeling (matrix metalloproteinases 3/9/10, urokinase receptor), endothelial activation (E-selectin), T-cell activation (IL2RA), neutrophil activation (myeloperoxidase), lipid metabolism (FABP4), and growth factors (FGF21, transforming growth factor-α).
By allelic copy number analysis at missense single-nucleotide polymorphisms on 26 genes with copy number variation, we identified a significant association between atopic dermatitis and human KPRP.
Combination treatment with lipoteichoic acids isolated from Lactobacillus plantarum and Staphylococcus aureus alleviates atopic dermatitis via upregulation of CD55 and CD59.
Basophils were accumulated in the inflamed skin of IL33tg mice, and AD-like inflammation was alleviated by the conditional depletion of basophils using anti-FcεRIα antibodies or a Bas-TRECK transgenic mouse system.
In vitro AD analysis of these two polymers showed significant inhibition against the release of β-hexosaminidase and tumor necrosis factor (TNF-α) from RBL-2H3 cells.
Previously, we detected that 14-3-3 protein epsilon (YWHAE) was involved in the pathogenesis of atopic dermatitis (AD) and tyrosinase-mediated pigmentation.
To assess the relation between the total IgE (tIgE) and asIgE targeted against SEA (SEA-sIgE) and SEB (SEB-sIgE), as indicators of the severity of the course of AD, and the presence of S. aureus on apparently healthy skin, in skin lesions and in the nasal vestibule.
COX1 and ALOX12B expression, COX and 12/15-LOX metabolites as well as various lipids, which are known to induce itch (12-HETE, LTB4, TXB2, PGE2 and PGF2) and the ratio of pro-inflammatory vs pro-resolving lipid mediators in non-affected and affected skin as well as in the serum of AD patients were increased, while n3/n6-PUFAs and metabolite ratios were lower in non-affected and affected AD skin.
A T cell-intrinsic increase of gp130 expression upon Ets1 deficiency promotes the gp130-mediated IL-6 signaling pathway, thereby leading to the development of severe AD-like symptoms.
The pathogenic role of staphylococcal enterotoxins in adult AD can be explained by their ability to downmodulate the activated effector T cell response, altering gene expression profile such as EGR2 induction, and may contribute to negative regulation of polyfunctional CD4<sup>+</sup> T cells in these patients.
The AnxA1<sup>-/-</sup> AD group exhibited skin with intense erythema, erosion and dryness associated with increased skin thickness compared to the AD WT group.