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ATOPIC DERMATITIS MODEL ANIMAL AND USE THEREOF 新技術説明会

外国特許コード F150008351
整理番号 S2013-0593-C0
掲載日 2015年6月11日
出願国 世界知的所有権機関(WIPO)
国際出願番号 2014JP061931
国際公開番号 WO 2014178392
国際出願日 平成26年4月30日(2014.4.30)
国際公開日 平成26年11月6日(2014.11.6)
優先権データ
  • 特願2013-096637 (2013.5.1) JP
発明の名称 (英語) ATOPIC DERMATITIS MODEL ANIMAL AND USE THEREOF 新技術説明会
発明の概要(英語) Provided are a transgenic nonhuman mammal that holds a DNA encoding IL-33 in a state of being expressible specifically in the skin, etc., when fed under specific pathogen free (SPF) conditions, said transgenic nonhuman mammal having, compared with a non-transgenic nonhuman mammal corresponding thereto, one or more characteristics selected from the group consisting of: (1) spontaneously developing dermatitis; (2) showing an increase in inflammatory cell count; (3) showing an increase in total IgE concentration, histamine concentration, cytokine concentration and/or chemokine concentration; and (4) showing an increase in scratching behavior time.
従来技術、競合技術の概要(英語) BACKGROUND ART
Atopic dermatitis is, pruritic, chronic inflammatory skin disorder and repetitive, have a genetic background, with a high level in the blood serum IgE and. In addition, eosinophils and mast cells at the lesion site is collected, blood eosinophils also increases. The onset mechanism of atopic dermatitis is still not completely elucidated, cell activation T, on mast cells or basophils bound immunoglobulin Fc ε R (hereinafter, referred to as Ig) cross linking of the molecules E induced by mast cells and basophils consequence of the activation of, chemical mediators and cytokines associated with the generation of Th2 occurs is considered important. The cytokines, interleukins (hereinafter, referred to as IL) -4, IL-13, and IL-5, chemical mediators and histamine, serotonin and the like. In this case, in particular the activation of mast cells and basophils is antigen-specific IgE is an important role, antigen specificity is not apparent in the case of natural type atopic dermatitis, is not limited to, an external stimulus and infections, such as IL-18 is implicated, details remain unknown.
Genetically engineered atopic dermatitis model mouse as the system 7 'IL-4 Tg, CASP1 Tg, IL-18 Tg, IL-31 Tg, Re1B-KO, (non-patent document 1) CatE-KO, MAIL-KO(non-patent document 2) ' is reported.
However, produced by genetically engineered mouse model of atopic dermatitis is atopic dermatitis actually does not always reflect the feature. For example, produced by genetic engineering atopic dermatitis model was reported as some of the model, high expression of the gene is localized in the patient's skin to atopic dermatitis enhanced expression of a gene not normally found in a model (CASP1 Tg, IL-18 Tg, IL-4 Tg), dermatitis or tissue eosinophils in neutrophil but also, with no change to the value of the IgE (IL-31 Tg), with characteristics such as human atopic dermatitis model to appropriately reflect the disease is not necessarily considered. In addition to the mice do not exhibit symptoms Pruritus RelB-KO, MAIL - KO mice (IkB ζ) perinatal mortality rate is very high, the high stringency condition is inflammation such as in terms of atopic dermatitis model is incomplete. Therefore, these model mice of atopic dermatitis in the case of using the evaluation, there is a concern that does not reflect the actual condition.
However, in recent years include atopic dermatitis research progresses, new knowledge has been created. Recently, atopic dermatitis skin of the patient's skin keratinocytes in the nuclei of the cells, an increased expression level of IL-33 has been reported (non-patent document 3). IL-33 IL-1β IL-18 and is highly homologous with the amino acid sequence identified as belonging to the family cytokine IL-1 is, ST2 to its receptor. ST2 Th2 Of the cells involved in the cell or allergy (basophils, mast cells, eosinophils, natural type 2 lymphocytes) can be expressed on, Th2 is involved in a disease of allergy IL-33 is suggested. However, mouse recombinant IL-33 directly administering locally within the dermis of the skin and, associated with increased dermal collagen fibers scleroderma-like reaction occurs, with or without the change of the epidermis (non-patent document 4) and reported to, epidermal thickening with psoriasis-like skin (non-patent document 5) occurs and a report that the, the influence on the skin of the IL-33 is not clear. Under the present circumstances such, until now IL-33 highly expressed in the skin in a transgenic animal that is not present, their phenotype was also remain unclear.
  • 出願人(英語)
  • ※2012年7月以前掲載分については米国以外のすべての指定国
  • HYOGO COLLEGE OF MEDICINE
  • MIE UNIVERSITY
  • 発明者(英語)
  • YAMANISHI, Kiyofumi
  • MIZUTANI, Hitoshi
  • IMAI, Yasutomo
  • YOSHIMOTO, Tomohiro
  • NAKANISHI, Kenji
国際特許分類(IPC)
指定国 National States: AE AG AL AM AO AT AU AZ BA BB BG BH BN BR BW BY BZ CA CH CL CN CO CR CU CZ DE DK DM DO DZ EC EE EG ES FI GB GD GE GH GM GT HN HR HU ID IL IN IR IS JP KE KG KN KP KR KZ LA LC LK LR LS LT LU LY MA MD ME MG MK MN MW MX MY MZ NA NG NI NO NZ OM PA PE PG PH PL PT QA RO RS RU RW SA SC SD SE SG SK SL SM ST SV SY TH TJ TM TN TR TT TZ UA UG US UZ VC VN ZA ZM ZW
ARIPO: BW GH GM KE LR LS MW MZ NA RW SD SL SZ TZ UG ZM ZW
EAPO: AM AZ BY KG KZ RU TJ TM
EPO: AL AT BE BG CH CY CZ DE DK EE ES FI FR GB GR HR HU IE IS IT LT LU LV MC MK MT NL NO PL PT RO RS SE SI SK SM TR
OAPI: BF BJ CF CG CI CM GA GN GQ GW KM ML MR NE SN TD TG

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