Expression of keratin 1, keratin 10, desmoglein 1 and desmocollin 1 in the epidermis: possible downregulation by interleukin-4 and interleukin-13 in atopic dermatitis

Totsuka, Ami; Omori‐Miyake, Miyuki; Kawashima, Makoto; Yagi, Junji; Tsunemi, Yuichiro

doi:10.1684/ejd.2017.2985

Cited by 43 publications

(31 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The expression of Desmocollin-1 ( Dsc-1 ), a marker gene for keratinocytes, can correlate with normal epidermal differentiation and development of keratinocytes ( 21 ). Additionally, the presence of IL-4 has been shown to downregulate the expression of Dsc-1 ( 22 , 23 ). We therefore examined whether keratinocyte function would be altered due to loss of IL-4Rα on keratinocytes by measuring Dsc-1 expression and treating with recombinant IL-4.…”

Section: Resultsmentioning

confidence: 99%

Deletion of Interleukin-4 Receptor Alpha-Responsive Keratinocytes in BALB/c Mice Does Not Alter Susceptibility to Cutaneous Leishmaniasis

et al. 2018

View full text Add to dashboard Cite

show abstract

Section: Resultsmentioning

confidence: 99%

Deletion of Interleukin-4 Receptor Alpha-Responsive Keratinocytes in BALB/c Mice Does Not Alter Susceptibility to Cutaneous Leishmaniasis

et al. 2018

View full text Add to dashboard Cite

show abstract

“…We also confirmed that CAPS administration lowered IL-4 transcription. IL-4 is the key cytokine of Th-2 type cytokines [ 24 ]. These results support our hypothesis.…”

Section: Discussionmentioning

confidence: 99%

Effect of administrating polysaccharide from black currant (<i>Ribes nigrum</i> L.) on atopic dermatitis in NC/Nga mice

Ashigai

Komano

Wang

et al. 2018

Bioscience of Microbiota, Food and Health

View full text Add to dashboard Cite

Atopic dermatitis (AD) is a chronic inflammatory skin disease that causes dry skin and functional disruption of the skin barrier. AD is often accompanied by allergic inflammation. AD patient suffer from heavy itching, and their quality of life is severely affected. Some pharmaceuticals for AD have some side effects such as skin atrophy. So it is necessary to develop mild solutions such as food ingredients without side effects. There are various causes of AD. It is especially induced by immunological imbalances such as IFN-γ reduction. IFN-γ has an important role in regulating IgE, which can cause an allergy reaction. NC/Nga mice develop AD and IgE hyperproduction. In a previous study, we revealed that administration of polysaccharide from black currant (R. nigrum) has an effect on immunomodulation. It induces IFN-γ production from myeloid dendritic cells. We named this polysaccharide cassis polysaccharide (CAPS). In this report, we studied the effect of administering CAPS on atopic dermatitis in NC/Nga mice. Thirty NC/Nga mice that developed symptoms of atopic dermatitis were used. We divided them into three groups (control, CAPS administration 12 mg/kg/day, CAPS administration 60 mg/kg/day). For 4 weeks, we evaluated clinical score, serum IgE levels, gene expression of spleen, and skin pathology. We revealed that CAPS administration improves atopic dermatitis symptoms. We also found that CAPS administration suppresses IgE hyperproduction and induces IFN-γ gene transcription in the spleen. Finally, we confirmed that CAPS administration suppresses mast cell migration to epidermal skin. These results indicated that CAPS has an effect on AD.

show abstract

“…AD skin is characterized by broad defects in terminal keratinocyte differentiation (ref. 61 and Figure 3), expansion of cells in the SB layer, and concomitant reduction in cells of the SS and SG layers (62,63). Hyperproliferating epithelium is associated with KRT6/16 overexpression (64).…”

Section: Failure Of Terminal Keratinocyte Differentiation In Ad Skinmentioning

confidence: 95%

Epithelial barrier repair and prevention of allergy

Goleva¹,

Berdyshev

Leung

2019

Journal of Clinical Investigation

154

173

View full text Add to dashboard Cite

Allergic diseases such as atopic dermatitis (AD), food allergy (FA), asthma, and allergic rhinitis affect more than 30% of the population (1-3). These diseases have in common a dysfunctional epithelial barrier, resulting in the penetration of allergens and microbes, accompanied by the release of epithelial-derived cytokines (e.g., thymic stromal lymphopoietin [TSLP], IL-25, IL-33), which drive type 2 immune responses. Although other immune pathways can modify the course of illness, cytokines including IL-4, IL-13, IL-31, TSLP, and IL-33 play a key role in allergic diseases (4-8), eliciting local tissue injury and repair (5,(9)(10)(11)(12)(13)(14).AD is the most prevalent chronic inflammatory skin disease (3,(15)(16)(17)(18)(19). In a subset of allergic patients, it is thought that ADrelated skin epithelial dysfunction contributes to the atopic march, which starts with AD and often leads directly to FA (20-23). The link from AD to respiratory allergy is more controversial; however, atopic march progression is facilitated in patients who develop IgE to both food and inhalant allergens (24).In this Review, we describe formation of the skin barrier, review the link between altered skin barrier formation and AD, discuss evidence for epithelial barrier dysfunction in other allergic diseases, and explore epithelial barrier intervention/repair strategies with the goal of preventing AD and the atopic march. The cornified envelope and keratinocyte differentiation in the skinThe skin's barrier function primarily depends on the outermost epidermal layer, stratum corneum (SC). To form SC, keratinocytes pass through a tightly regulated differentiation program and sequentially form stratum basale (SB), stratum spinosum (SS), stratum granulosum (SG), and SC layers of the skin (Figure 1). In human skin, keratinocytes irreversibly exit the cell cycle after mitosis in the basal layer and differentiate progressively across the epidermis toward the SC. Each layer is defined by its expression of characteristic morphological and biochemical features indicating its state of differentiation (25-27). The keratins KRT5 and KRT14 are predominantly expressed by basal keratinocytes. The markers of early differentiation KRT1 and KRT10 are made in SS. The cornified envelope precursors involucrin (IVL) and transglutaminase-1 (TGM1) are also present in SS. Late differentiation markers including the cornified envelope protein loricrin (LOR) and the precursor of the keratin cross-linking protein filaggrin (FLG) are expressed in SG keratinocytes. TGM1 cross-links IVL, LOR, and other structural proteins to form the cornified envelope.Calcium forms a steep gradient across the human epidermis, increasing from the SB (5 μM) to the outer SG (>20 μM) (27, 28). Importantly, there is cell-to-cell heterogeneity in average Ca 2+ concentrations in the epidermis (28). Formation of the Ca 2+ gradient coincides with key developmental milestones of skin barrier formation and differentiation into the SC.Primary human keratinocyte cultures are an excellent model for...

show abstract

Expression of keratin 1, keratin 10, desmoglein 1 and desmocollin 1 in the epidermis: possible downregulation by interleukin-4 and interleukin-13 in atopic dermatitis

Cited by 43 publications

References 28 publications

Deletion of Interleukin-4 Receptor Alpha-Responsive Keratinocytes in BALB/c Mice Does Not Alter Susceptibility to Cutaneous Leishmaniasis

Deletion of Interleukin-4 Receptor Alpha-Responsive Keratinocytes in BALB/c Mice Does Not Alter Susceptibility to Cutaneous Leishmaniasis

Effect of administrating polysaccharide from black currant (<i>Ribes nigrum</i> L.) on atopic dermatitis in NC/Nga mice

Epithelial barrier repair and prevention of allergy

Contact Info

Product

Resources

About