Project/Area Number |
04405007
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Research Category |
Grant-in-Aid for General Scientific Research (A)
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Allocation Type | Single-year Grants |
Research Field |
広領域
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Research Institution | JICHI MEDICAL SCHOOL |
Principal Investigator |
YAOITA Hideo Jichi Medical School, 医学部, 教授 (00010249)
|
Co-Investigator(Kenkyū-buntansha) |
KIYOSAWA Tomoharu Jichi Medical School, 医学部, 病院助手 (90221217)
YAMANE Yasuhiro Jichi Medical School, 医学部, 病院助手 (70220431)
MURATA Satoru Jichi Medical School, 医学部, 助手 (70254919)
SUZUKI Masayuki Jichi Medical School, 医学部, 助手 (40171251)
KATAYAMA Hiroshi Jichi Medical School, 医学部, 講師 (50142401)
出光 俊郎 自治医科大学, 医学部, 助手 (20237027)
北島 康雄 自治医科大学, 医学部, 助教授 (70111797)
狩野 俊幸 自治医科大学, 医学部, 病院助手 (10204596)
|
Project Period (FY) |
1992 – 1994
|
Project Status |
Completed (Fiscal Year 1994)
|
Budget Amount *help |
¥22,500,000 (Direct Cost: ¥22,500,000)
Fiscal Year 1994: ¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1993: ¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 1992: ¥18,000,000 (Direct Cost: ¥18,000,000)
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Keywords | bullous diseases / autoimmune / IgG subclass / complements / adhesion molecules / signal transduction / cytoskeleton / cell to cell, cell to stroma interaction / 水疱症 / 自己免疫 / 接着分子 / IgG Subclass / 補体 / Signal transduction / cytoskelton / cell to cell cell to stroma interaction / 自己免役 / chemotaxis / cell to cell interaction / 細胞骨格 |
Research Abstract |
There are two types of bullous diseases, such as autoimmune bullous diseases and congenital bullous diseases. As for the autoimmune diseases we could get some evidences that some sort of signal transduction must occur in the keratinocyte after the bullous diseases auto-antibodies bind to the antigens which are the adhesion molecules. (1994, JD,1994 annual meeting for bullous diseases, 1995 JID in preparation). To our knowledge, this is the first evidence in the world. Also we found the differences of the function between the IgG subclasses of the antibodies. (1994 Autoimmunity, 1995 in preparation). Taken together, We are getting the first evidences of the new mechanism for the bullous diseases and of the new type of reaction in the immunology. As for the congenital bullous diseases We found the disturbance of keratin filaments (1989 Arch Dermatol Res) which lead to the discovery of keratin gene defects(1992 JID) and a patient with new type of the disease (1993 Br J.Dermatol, 1995 in preparation). As for the matter related to the both type of the bullous diseases, we found the new type of disturbance of keratin filaments which is not related to keratin gene defects but related to desmosome destruction, (1992 JDS). In another words, We are getting the first evidences of the functional relationship between desmosome and keratin, which may lead to the discovery of a new type of adhesion molecules. We also got the evidence of keratinocyte origin of proteoglycan in the basement membrane of epidermal-dermal junction which must be important in bullous diseases. (1995 sent to JID). These findings help to understand cell to stroma interaction
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