Keio University

Kose Corporation

Masayuki Amagai

Shigeo Koyasu

Takeji Nishikawa

Harumi Suzuki

Hiroshi Kawasaki

Kazuyuki Tsunoda

Makoto Mizuno

Keisuke Nagao

Miki Ito

Eiryo Kawakami

Keita Koseki

Tamotsu Ebihara

Akiharu Kubo

Eiji Naru

Toru Atsugi

Yukako Kimura

An estimation method for estimating a parameter related to skin function is provided. The estimation method includes an image acquisition step for acquiring a skin image in which unevenness of a skin surface is captured; an extraction step for extracting a feature vector based on topological information on the skin image from the skin image acquired in the image acquisition step; an estimation step for estimating the parameter related to skin function based on the feature vector extracted in the extraction step, using an estimation model constructed based on past actual measurement data in which feature vectors are associated with the parameter related to skin function; and a presentation step for presenting the parameter related to skin function estimated in the estimation step.

Estimation method, estimation model generation method, program, and estimation device

The object of the present invention is to provide a mouse model for allergic diseases such as atopic dermatitis, and a dermatitis mouse model with impaired skin-barrier function. The present inventors found out that a mouse that has been caused to completely lose the function of expressing profilaggrin protein and filaggrin protein by entirely or partially disrupting the endogenous gene encoding filaggrin by a genetic mutation such as deletion or replacement, can be used as a mouse model for allergic diseases or atopic dermatitis wherein the skin-barrier function has been impaired.

Allergic disease model animals

Pemphigus vulgaris (PV) is an autoimmune disease with a possible fatality of the skin and mucosae which is induced by an antibody against desmoglein 3 (Dsg3). Persistent production of anti-Dsg3 IgG can be induced by adoptively transferring spleen cells of a DSG3&#x2212;/&#x2212; mouse immunized with rDsg3 into an RAG2&#x2212;/&#x2212; immunodeficient mouse expressing Dsg3 protein. This IgG in the blood binds to the Dsg3 protein in vivo, induces the breakage of intercellular adhesion of keratinocytes and thus brings about the phenotype of pemphigus vulgaris involving the formation of blisters in the oral mucosa and the disappearance of resting hair. These effects are sustained over 6 months. By using this method, active disease model animals relating to various autoimmune diseases can be constructed.

Autoimmune disease model animal

The present invention provides a monoclonal antibody having a pathogenic activity that can induce pemphigus lesion, a peptide specifically recognized by the monoclonal antibody and useful as a therapeutic drug for pemphigus autoimmune disease, etc. As anti-mouse Dsg3 antibody-producing cells are present in the splenocytes of pemphigus vulgaris mouse model constructed by using autoantigen knockout mouse, cell fusion was conducted with the splenocytes of said mouse model and mouse myeloma cells using polyethyleneglycol, hybridomas were constructed, and monoclonal antibodies against Dsg3 were constructed. Among them, a monoclonal antibody having a pathological activity that can induce pemphigus lesions was screened, the base sequence and amino acid sequence in its variable region (heavy chain, light chain) was determined, and the specific epitope part was identified.

Pemphigus monoclonal antibody

(PV) is an autoimmune disease with a possible fatality of the skin and mucosae which is induced by an antibody against desmoglein 3 (Dsg3). Persistent production of anti-Dsg3 IgG can be induced by adoptively transferring spleen cells of a DSG3&#x2212;/&#x2212; mouse immunized with rDsg3 into an RAG2&#x2212;/&#x2212; immunodeficient mouse expressing Dsg3 protein. This IgG in the blood binds to the Dsg3 protein in vivo, induces the breakage of intercellular adhesion of keratinocytes and thus brings about the phenotype ofinvolving the formation of blisters in the oral mucosa and the disappearance of resting hair. These effects are sustained over 6 months. By using this method, active disease model animals relating to various autoimmune diseases can be constructed.

Growing community of inventors

Tokyo, Japan

Masayuki Amagai