089 Energy sensor, stress-induced mTOR inhibitor REDD1 controls response to allergic contact dermatitis

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Regulation of mTOR and cell growth in response to energy stress by REDD1.

The tuberous sclerosis tumor suppressors TSC1 and TSC2 regulate the mTOR pathway to control translation and cell growth in response to nutrient and growth factor stimuli. We have recently identified the stress response REDD1 gene as a mediator of tuberous sclerosis complex (TSC)-dependent mTOR regulation by hypoxia. Here, we demonstrate that REDD1 inhibits mTOR function to control cell growth i...

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INTRODUCTION Contact dermatitis to cosmetics is a common problem in the general population, although its prevalence appears to be underestimated. We reviewed cases of allergic contact dermatitis to cosmetics diagnosed in our dermatology department over a 7-year period with a view to identifying the allergens responsible, the frequency of occurrence of these allergens, and the cosmetic products ...

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Allergic Contact Dermatitis Induced by Textile Necklace

Allergic contact dermatitis to textile dyes is considered to be a rare phenomenon. A recent review reported a prevalence of contact allergy to disperse dyes between 0.4 and 6.7%. The relevance of positive patch testing was not reported in all studies. Textile dye allergy is easily overlooked and is furthermore challenging to investigate as textile dyes are not labelled on clothing. In this repo...

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TRPA1 controls inflammation and pruritogen responses in allergic contact dermatitis.

Allergic contact dermatitis is a common skin disease associated with inflammation and persistent pruritus. Transient receptor potential (TRP) ion channels in skin-innervating sensory neurons mediate acute inflammatory and pruritic responses following exogenous stimulation and may contribute to allergic responses. Genetic ablation or pharmacological inhibition of TRPA1, but not TRPV1, inhibited ...

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Allergic Contact Dermatitis Physiology

Allergic Contact Dermatitis (ACD) involves the penetration of an allergen through the skin surface where it acts as a hapten by binding to epidermal proteins and eliciting, a delayed Type IV hypersensitivity reaction 48 to 120 hours after exposure. This immunologic response involves the activation of Th1 cells with the subsequent release of cytokines resulting in the classic inflammatory reaction.

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ژورنال

عنوان ژورنال: Journal of Investigative Dermatology

سال: 2019

ISSN: 0022-202X

DOI: 10.1016/j.jid.2019.03.165