Publications by authors named "Kerstin Ahrens"

The proteolytic regulation of the desquamation process by kallikrein-related peptidases (KLKs) is crucial for epidermal barrier function, and elevated KLK levels have been reported in atopic dermatitis. KLKs are controlled by specific inhibitors of the serine protease inhibitor of Kazal-type (Spink) family. Recently, SPINK6 was shown to be present in human stratum corneum.

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The S100 fused-type proteins (SFTPs) are thought to be involved in the barrier formation and function of the skin. Mutations in the profilaggrin gene, one of the best investigated members of this family, are known to be the major risk factors for ichthyosis vulgaris and atopic dermatitis. Recently, we identified human filaggrin-2 as a new member of the SFTP family.

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Article Synopsis
  • β-Defensins, particularly murine β-defensin-14 (mBD-14), are antimicrobial peptides produced in the skin in response to stimuli like UV radiation, bacterial infections, and inflammatory signals.
  • Research shows that mBD-14 can convert certain CD4(+) T cells into regulatory T cells (Tregs), enhancing their ability to suppress immune responses, which could help prevent allergies or overreactions in the immune system.
  • The study indicates that mBD-14 promotes Treg formation through mechanisms involving IL-10 but does not affect dendritic cells, suggesting that while it contributes to immune regulation, it does not play a significant role in UV-induced immunosuppression.
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It has been suggested that the increased rate of bacterial infection in atopic dermatitis (AD) may be caused by reduced antimicrobial protein (AMP) expression. We were interested whether common treatments in AD affect antimicrobial defense. We investigated the effects of topically applied corticosteroids betamethasone valerate (BV) and triamacinolone acetonide (TA) and those of the calcineurin inhibitor pimecrolimus for 3 weeks on AMP expression in AD.

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Protection of the skin against microbiological infection is provided by the permeability barrier and by antimicrobial proteins. We asked whether the expression of murine β-defensins (mBDs)-1, -3, and -14-orthologs of human β-defensins hBD-1, -2, and -3, respectively--is stimulated by mechanically/physicochemically (tape stripping or acetone treatment) or metabolically (essential fatty acid-deficient (EFAD) diet) induced skin barrier dysfunction. Both methods led to a moderate induction of mBD-1 and mBD-14 and a pronounced induction of mBD-3 mRNA.

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