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this study shows that MyD88 signaling in T regulatory cells by endogenous ligands dampens skin inflammation in filaggrin deficient mice
We show that filaggrin-deficient flaky tail (ft/ft) mice have an increased number of gammadeltaT17 cells in the spleen, epidermis, and thymus compared to wild-type mice.
Findings suggest that Flg mutation causes the decrease in sweating in the murine model.
Loss of epidermal AP1 reduces filaggrin level, alters chemokine expression and produces an ichthyosis-related phenotype.
increased activity of the PI3K/AKT signaling pathway in Pelo-deficient skin might conflict with the dephosphorylation of profilaggrin and thereby affect its proper processing into filaggrin monomers and ultimately the epidermal differentiation
mutations may predispose to skin disease in young children including urticaria, and rash not recognized as atopic dermatitis although equally frequent
Filaggrin deficiency did not affect the epidermal tight junction barrier directly, but once dermatitis occurred, the skin inflammation induced TJ dysfunction
Filaggrin deficiency promotes the dissemination of cutaneously inoculated vaccinia virus.
Hypoxic treatment of primary keratinocytes induced filaggrin (Flg) gene expression in a HIF1alpha- and HIF2alpha-dependent manner.
increased expression in keratinocytes attenuated the development of atopic dermatitis-like skin inflammation
the a/a ma ft/ma ft/J mouse model can be used as an appropriate model to study early AD onset associated with profilaggrin deficiency.
Mere impairment of filaggrin degradation by loss of caspase 14 does not influence the inflammatory threshold of atopic dermatitis.
Complete filaggrin deficiency led to altered barrier integrity and enhanced sensitization, which are important factors in early-phase atopic dermatitis.
The decreased expression of epidermal growth factor receptor (EGFR), E-cadherin, occludin, and SIRT1 in the skin of Flg(ft) mice, compared with those in C57BL/6J mice, is reported.
Atopic dermatitis (AD) with Filaggrin (FLG) mutations is associated with an increased SC IL-1 cytokine profile; this profile is also seen in a murine homologue of filaggrin deficiency.
the filaggrin-histidine-urocanic acid pathway is not essential for stratum corneum acidification
ELA2 localized to keratohyalin granules, where it was found to directly participate in (pro-)filaggrin processing.
complete sequence of the gene; significant homology between the mouse and human filaggrin promoter sequences and in the calcium-binding domain, but the remainder of the protein-coding region shows substantial divergence.
Immunoreactivity of filaggrin, which is the main precursor of free amino acids in the stratum corneum, became faint in the epidermis of the mice transferred from a humid or normal to a dry environment.
Keratinocyte Matriptase/MT-SP1 as an essential component of the profilaggrin-processing pathway and a key regulator of terminal epidermal differentiation.
When skin barrier bypass is excluded, there is a significant association between polysensitivity and filaggrin loss-of-function mutations.
This study shows that the heterozygous S2889X mutation is frequent in Indian hand eczema patients. We also observed that FLG mutations (S2889X and 2282del4) are significantly associated with irritant contact dermatitis with or without atopy, allergic contact dermatitis without atopy, and idiopathic subtypes of hand eczema.
Study found no influence of common FLG mutations on changes in epidermal Langerhans cells (LC) and monocyte numbers, LC activation or related cytokine levels in the ultraviolet B irradiated skin.
Study suggests that FLG mutations are a significant predisposing factor for food allergies in Japanese primary school students and may influence the persistence of food allergies from infancy to the primary school years.
Epistasis between immune (IL4R) and skin (FLG) regulatory genes exist in the pathogenesis of allergic sensitization. Hence, genetic susceptibility towards defective epidermal barrier and deviated immune responses could work together in the development of allergic sensitization.
rare putative loss-of-function allele in FLG was identified as a major component of atopic eczema susceptibility in the Bangladeshi cohort
FLG-LOF mutations are a significant risk factor for later childhood asthma and rhinitis. However, the pathway to asthma is only through early childhood eczema while a direct effect was observed for childhood rhinitis.
Array-based sequencing of filaggrin gene for comprehensive detection of disease-associated variants.
results demonstrate that GATA3 is involved in the regulation of filaggrin and filaggrin-2 expression during inflammatory conditions in the skin.
We discovered 2 pathogenic FLG LOF not previously reported for AD (c.488delG and p.S3101*). The overlap of our p.S3316* findings in our cohort, in an independent AA AD study, and in African individuals (ExAC, ESP, and 1000G) supports p.S3316* as a population-specific FLG LOF variant for African ancestry.
Microbiome composition in AD nonlesional skin is associated with FLG mutations, proposing a possible association between the skin microbiome and host genetics.
In contrast to previous reports, uncommon FLG loss of function (LoF) variants in African American children exist and are associated with atopic dermatitis and more persistent disease. In contrast to Europeans, no FLG LoF variants predominate in African American children.
There was no correlation between nickel on the skin surface or nickel penetrating into the stratum corneum at any time points and FLG mutation status, self-reported hand dermatitis, or a history of atopic dermatitis.
There was a significant correlation between palmar hyperlinearity and Filaggrin null mutations, especially over age 2 years
The results suggest that filaggrin mutations may have a negative impact on the success of immunosuppressive treatment in severe atopic dermatitis.
The present study demonstrated that children without loss-of-function gene mutations for the epidermal barrier protein filaggrin showed clearer effects of indoor environmental factors on childhood eczema and wheeze.
In our study, in the AD and IV patients, loss-of-function FLG mutation was not found. This means that another mechanism other than FLG nonsense mutation is involved in the pathogenesis of these patients.
The frequency of FLG copy number variation (CNV) alleles (CNV10 was lower among hairdressers than controls, which may indicate a healthy worker selection. Moreover, FLG null and CNV10 were associated with cancer-related DNA changes in hairdressers, which may influence their risk of cancer.
Filaggrin regulates epidermal terminal differentiation and impairs MAPK signaling pathway in normal human epidermal keratinocytes.
The authors found 11 frameshift variants and 14 nonsense variants in this Han Chinese population. The results increase the spectrum of IV variants.
The protein encoded by this gene is an intermediate filament-associated protein that aggregates keratin intermediate filaments in mammalian epidermis. It is initially synthesized as a polyprotein precursor, profilaggrin (consisting of multiple filaggrin units of 324 aa each), which is localized in keratohyalin granules, and is subsequently proteolytically processed into individual functional filaggrin molecules. Mutations in this gene are associated with ichthyosis vulgaris.
, keratin intermediate filament-associated protein
, epidermal filaggrin
, Filaggrin (profilaggrin)