Recently, the spontaneous production of intracellular interferon-gamma (IFN-gamma) and spontaneous secretion of IL-6 has been documented in patients with atopic dermatitis.
To evaluate and characterise the therapeutic effects of human Wharton's jelly-derived MSCs (WJ-MSCs) primed with the Toll-like receptor 3 agonist poly I:C or interferon-γ (IFN-γ) in a murine model of AD.
An opposite effect was detected upon IFN-γ production in TCD4 cells, such that AD IgG reduced IFN-γ production compared to production under mock conditions but not under IVIG conditions.
These results suggest that IFN-γ decreases CERs with long-chain FAs through the downregulation of ELOVL and CerS and that this mechanism may be involved in the CER profile alteration observed in psoriasis and AD.
Reduced interferon-gamma (IFN-gamma) secretion with increased IFN-gamma mRNA expression in atopic dermatitis: evidence for a post-transcriptional defect.
Taken together, the lactobacilli isolated from <i>Jeotgal</i> may suppress the development of AD-like skin inflammation in mice by modulating IL-4 and IFN-γ production in CD4<sup>+</sup> T cells, presumably via enhancing IL-12 production by macrophages.
In the AD group, the levels of IL-18, IL-4, and IFN-γ in lymphocyte cultures with SEB were significantly increased compared with non-SEB exposed cells (each p<0.001); similar results were found in the control group.
Fluorescence‑activated cell sorting demonstrated that the population of CD4+/IL‑4+, CD4+/IFN‑γ+ and CD4+/IL‑17A+ cells in draining lymph nodes was also significantly decreased in AXE‑treated mice compared with AD mice without AXE treatment.
Here, we aimed to investigate whether pCpG-Muγ, a plasmid continuously expressing murine IFN-γ, is an effective treatment of atopic dermatitis, a Th2-dominant skin disease.
Furthermore, we found that eupatilin suppressed the levels of serum immunoglobulin E (IgE), interleukin-4 (IL-4), and AD involved cytokines, such as tumor necrosis factor α (TNFα), interferon-γ (IFN-γ), IL-1β, and thymic stromal lymphopoietin (TSLP), IL-33, IL-25 and increased the levels of filaggrin and loricrin in the oxazolone-induced AD-like mouse model.
Eight IRF2 SNPs were significantly associated with IFN-γ production after herpes simplex virus (HSV) stimulation (P = 0.048-0.0008), including an AD-associated SNP (rs13139310, P = 0.008).
Increases of general inflammatory (IL-2), innate (IL-1β), and some T<sub>H</sub>1/interferon (IFN-γ) markers in patients with ichthyosis were comparable with those in patients with psoriasis or AD.
Treatment of GCSE significantly reduced IgE production and expression of AD associated pathogenic cytokines such as IL-4, IL-5, IL-10, IL-13, IL-17, TNF-α, and IFN-γ by lymphocytes isolated from AD-induced mice.
AD-MSCs showed an upregulation of many Th1/Th17 cytokines [interleukin (IL)-6, IL-8, IL-12, IL-13, IL-17A, IL-17F, transforming growth factor-β, interferon-γ], while Th2 chemokines (IL-2, IL-4, IL-5, IL-23A) were downregulated in AD-MSCs.
In this study, we used in situ hybridization to investigate the expression of interleukin 4 (IL-4), IL-5, and interferon-gamma (IFN-gamma) messenger RNA (mRNA) in skin biopsies from acute and chronic skin lesions of patients with AD.
In conclusion, the imbalance in IL-4 and IFN-gamma secretion in patients with atopic dermatitis may reflect general T cell activation in the presence of an intrinsic defect of IFN-gamma secretion.
These results suggest that CG inhibited the development of the AD-like skin symptoms by modulating Th1 and Th2 responses in the skin lesions in mice and TARC expression by suppressing TNF-α/IFN-γ-induced NF-κB activation in keratinocytes, and so may be a useful tool in the therapy of AD-like skin symptoms.
We show that miR-146a expression is increased in keratinocytes and chronic lesional skin of patients with AD. miR-146a inhibited the expression of numerous proinflammatory factors, including IFN-γ-inducible and AD-associated genes CCL5, CCL8, and ubiquitin D (UBD) in human primary keratinocytes stimulated with IFN-γ, TNF-α, or IL-1β.