Furthermore, depletion of the microbiota through the oral administration of antibiotics (ABX) partially rescued both the skin inflammation and systemic inflammation, demonstrating a role for the gut microbiota in SHARPIN-deficient mice.
Identification and rapid monitoring of these lipids represent a tool to assess therapeutic outcomes in SHARPIN-deficient mice and other mouse models of dermatitis and may have diagnostic utility in atopic dermatitis.
Loss of one Ripk1 allele limited lesion formation and significantly extended the lifespan of cIap1<sup>EKO/EKO</sup>.cIap2<sup>-/-</sup> mice. cIAP activities are important for recruitment of LUBAC to signaling complexes, and loss of LUBAC component SHARPIN, induces dermatitis in mice.
Mice with spontaneous mutations in the Sharpin gene develop chronic proliferative dermatitis that is characterized by eosinophilic inflammation of the skin and other organs with increased expression of type 2 cytokines and dysregulated development of lymphoid tissues.