Researchers Connect FADD Protein to Skin Inflammation

Researchers from the University of Cologne, Ghent University and the German Sport University Cologne have identified the protein that may stop necroptosis in keratinocytes, thereby preventing skin inflammation.

In "the Adaptor Protein FADD Protects Epidermal Keratinocytes from Necroptosis In Vivo and Prevents Skin Inflammation," an article published by Cell Press in the October issue of Immunity, the researchers identified that the Fas Associated Death Domain (FADD) protein interacts with "death receptors" to activate apoptosis. Death receptors have also been shown to induce necroptosis, a different type of cell death mediated by the proteins RIP1 and RIP3.

In their experiments, the researchers found that removing FADD in the epidermis of mice  showed spontaneous necroptosis of keratinocytes and developed severe inflammatory skin lesions within a few days of birth. Further, RIP3-dependent necrotic death of FADD-deficient keratinocytes was identified as the initiating event triggering skin inflammation.

It was therefore concluded that FADD allows keratinocytes to avoid necroptosis to prevent skin inflammation. Also, the researchers suggest that genetic or external factors sensitizing keratinocytes necroptosis could be implicated in the pathogenesis of skin inflammation, a feature of many chronic or acute skin conditions such as eczema, psoriasis and drug rashes.

Skin inflammation is an issue that affects a vast majority of consumers, both in the OTC and dermatology markets. A material that prevents FADD removal in epidermal keratinocytes could perhaps prevent skin inflammation in both instances.

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