The present disclosure, relates, in general, to methods of treating atopic dermatitis, including moderate or severe atopic dermatitis, and chronic atopic dermatitis, using an antibody specific for thymic stromal lymphopoietin (TSLP).

The present invention provides methods for treating atopic dermatitis (AD). Also provided are methods for improving one or more AD-associated parameter(s), and methods for decreasing the level of at least one AD-associated biomarker in a subject in need thereof. The methods of the present invention comprise administering to a subject in need thereof a pharmaceutical composition comprising an interleukin-4 receptor (IL-4R) antagonist such as an anti-IL-4R antibody.

Provided are methods and systems for determining functional relationships between ex vivo skin models and an inflammatory skin condition. Also provided are methods and systems for identifying modulators of inflammation of skin, as well as the use of modulators identified by such methods or systems for the preparation of cosmetic compositions, personal care products, or both.

The present disclosure provides methods for identifying agents that are candidate agents for treating atopic dermatitis. The present disclosure provides methods for diagnosing atopic dermatitis. The present disclosure provides compositions and methods for treating atopic dermatitis.

The presence of misfolded proteins in the brain is the hallmark of neurodegenerative diseases. Protein aggregates could have systemic expression and might be found in several tissues including the skin. This demonstrates the presence of phosphorylated Tau (p-Tau) in the skin cells of patients with Alzheimer's Disease (AD). Antibodies against p-Tau (PHF, phosphorylated at S296 and AT8, phosphorylated at S202) were assayed in biopsied tissue from the retro-auricular area in 49 subjects: 20 with AD, 12 with nondegenerative dementia and 17 age-matched controls. Light and confocal microscopies were employed to localize Tau protein by immunohistochemistry and their presence in the skin was confirmed through Western blots. The skin biopsy taken from AD patients presented significantly higher levels of p-Tau (AT8: hyperphosphorylated at Ser 202) when compared both to control subjects and patients with non-degenerative dementia (p<0.001). This study demonstrates the presence of p-Tau in skin biopsies by immunoreactivity. This procedure could be used to support the clinical diagnosis of AD in living patients.

Methods of treating subjects with atopic dermatitis, e.g., associated with mutations in the TMEM79 gene, using Wnt inhibitors, e.g., porcupine inhibitors.

A polypeptide contains laminin beta-4 and a carrier contains the polypeptide. An antibody, preferably autoantibody, is against laminin beta-4. Furthermore, use of the polypeptide, carrier or autoantibody for the diagnosis of a disease, and a method with the step of detecting an autoantibody against laminin beta-4 in a sample are described.

Provided are a method and a composition for preventing or treating atopic dermatitis through administration of monoclonal stem cells and a method for screening atopic dermatitis patients suitable for administration of monoclonal stem cells and predicting prognosis of patients. According to the method for the subfractionation culture and proliferation of stem cells of the disclosure, large quantities of desired monoclonal mesenchymal stem cells can be obtained in a short period of time through rapid proliferation of monoclonal mesenchymal stem cells. In addition, the monoclonal mesenchymal stem cells thus obtained can be administered to atopic dermatitis patients according to a prescribed administration cycle, guidelines, and dose to effectively ameliorate atopy symptoms in the patients. Moreover, by using a marker to identify patient groups particularly suitable for the treatment and selectively administering the monoclonal mesenchymal stem cells to the patient groups, an excellent therapeutic effect for atopic dermatitis can be achieved.

Provided are a marker for detecting the severity of atopic dermatitis, and a method for detecting the severity of atopic dermatitis using the marker. The method for detecting the severity of atopic dermatitis in a test subject comprises a step of measuring an expression level of at least one gene selected from the group of 9 genes consisting of CAPN1, NCOR2, PPP1R9B, PLP2, GRN, PPP1R12C, LOC146880, SLC31A1 and SYVN1 or an expression product thereof for a biological sample collected from the test subject.

A method to predict a propensity of an individual to develop atopic dermatitis is disclosed. The method, which involves use of biological markers, can also be used to evaluate the efficacy of a composition to treat atopic dermatitis.