The present invention relates to a method for producing an avatar mouse, which is an animal model of atopic dermatitis, and a method of screening a therapeutic agent for atopic dermatitis using the same. According to the present invention, it is possible to more effectively identify a patient-specific immune response by representing an immune response in an actual atopic dermatitis patient. Thus, the present invention is expected to be widely used in the development of a new immunotherapy system enabling tailored treatment.

This disclosure relates to a genetically modified rodent and use thereof as a rodent model. More specifically, this disclosure relates to rodent (e.g., mouse or rat) comprising a loss of function mutation in an endogenous Crnn (cornulin) gene, and to use of such a rodent animal as a rodent model of skin inflammation disorders (e.g., psoriasis).

Provided herein are several monoclonal antibodies that activate the adhesion activity of human and mouse E-cadherin, including the amino acid sequences for the CDRs that define the binding domains of each monoclonal antibody. Also described are methods of making these antibodies, as well as biologically functional fragments and derivatives thereof; and methods of using them in the treatment, prevention, and/or amelioration of disease and conditions characterized by disruption of normal cell adhesion and/or cell junctions. Specifically contemplated are methods and compositions for the treatment of cancer metastasis as well as inflammatory conditions (such as inflammatory bowel disease and airway inflammation).

Provided are genetically modified non-human animals that express a human or chimeric (e.g., humanized) IL33, and methods of use thereof.

The present invention relates to: a recombinant peptide in which a Mitochondria Localization Sequence (MLS) peptide and the Signal Transducer and Activator of Transcription 3 (STAT3) are fused to each other; a recombinant vector carrying a polynucleotide coding for the recombinant peptide; and a composition comprising the recombinant peptide or the recombinant vector as an active ingredient for prevention or treatment of autoimmune disease or inflammatory disease, wherein the recombinant peptide or the recombinant vector allows STAT3 to be overexpressed in the mitochondria to enhance the mitochondrial function, resulting in inhibiting the expression of inflammatory cytokines including IL-17, whereby the composition may be advantageously used for preventing or treating autoimmune disease or inflammatory diseases.

The invention belongs to the biopharmaceutical. It involves the role and mechanism of PCSK9 in inflammatory immune diseases, and the application of PCSK9 inhibitors to the preparation of drugs for the treatment of inflammatory immune diseases mediated by T cells. In particular, it involves the use of PCSK9 monoclonal antibody, PCSK9 interference RNA and PCSK9 small molecule inhibitors for treating psoriasis, atopic dermatitis, or urticaria. The invention uses psoriasis as an embodiment for the study of inflammatory and immune diseases. It is found that PCSK9 plays an important role in the treatment of inflammatory immune diseases. The PCSK9 monoclonal antibody, PCSK9 interference RNA, and PCSK9 small molecule inhibitor can be further developed for treating inflammatory immune-diseases, such as psoriasis with fewer adverse reactions, at low cost, and with good efficacy.

The present disclosure relates to a method for establishing an oral ulcer animal model with Yin-deficiency and fire-excess syndrome based on sleep deprivation, comprising the following steps of: burning buccal mucosa of a rat with phenol to cause a white injury, and obtaining the oral ulcer animal model after 24-48 h; placing the animal model in a sleep deprivation device for 2-7 days; wherein the device is composed of a mouse box in which a plurality of platforms with a diameter of 4-8 cm are arranged at an interval of 10-20 cm from each other; and water is filled among the platforms, and the platforms are about 0.1-2 cm higher than a water surface. The present disclosure overcomes the defects of single evaluation index, short model duration, and unconformity of etiology and clinic existed in the prior art.

The present disclosure relates to genetically modified non-human animals that express a human or chimeric (e.g., humanized) IL4R and/or IL4, and methods of use thereof.

Non-human animals comprising a human or humanized IL-4 and/or IL-4Rα nucleic acid sequence are provided. Non-human animals that comprise a replacement of the endogenous IL-4 gene and/or IL-4Rα gene with a human IL-4 gene and/or IL-4Rα gene in whole or in part, and methods for making and using the non-human animals, are described. Non-human animals comprising a human or humanized IL-4 gene under control of non-human IL-4 regulatory elements is also provided, including non-human animals that have a replacement of non-human IL-4-encoding sequence with human IL-4-encoding sequence at an endogenous non-human IL-4 locus. Non-human animals comprising a human or humanized IL-4Rα gene under control of non-human IL-4Rα regulatory elements is also provided, including non-human animals that have a replacement of non-human IL-4Rα-encoding sequence with human or humanized IL-4Rα-encoding sequence at an endogenous non-human C IL-4Rα locus. Non-human animals comprising human or humanized IL-4 gene and/or IL-4Rα sequences, wherein the non-human animals are rodents, e.g., mice or rats, are provided.

The present invention provides an antibody to a fibrosis-related molecule and medical application thereof. The antibody of the present invention is an antibody that binds to CHL1 protein and an antibody that neutralizes the binding of the CHL1 protein to a fibroblast.