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1992 Fiscal Year Final Research Report Summary

The mechanism of joint destruction and its protection in the rheumatoid arthritis

Research Project

Project/Area Number 03807095
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field Orthopaedic surgery
Research InstitutionShiga University of Medical Science

Principal Investigator

NISHIOKA Junichi  Shiga Univ.Med.Sci., Med.School, Associate Prof, 医学部, 助教授 (80115766)

Co-Investigator(Kenkyū-buntansha) KOMIYA Yasuhiro  Shiga Univ.Med.Sci., Med.School, Resident, 医学部, 医員
SAITO Jun  Shiga Univ.Med.Sci., Med.School, Instructor, 医学部, 助手 (50225710)
USHIYAMA Toshio  Shiga Univ.Med.Sci., Med.School, Resident, 医学部, 医員
IWASAKI Atsushi  Shiga Univ.Med.Sci., Med.School, Instructor, 助手 (00231168)
INOUE Koji  Shiga Univ.Med.Sci., Med.School, Assistant Professor, 医学部, 講師 (80213156)
Project Period (FY) 1991 – 1992
Keywordsrheumatoid arthritis / joint destruction / IgE-receptor / arthritic marker / histochemistry / Synovium / lining cell / B-Lymphocyte
Research Abstract

The IgE receptor (Fce RII) is suggested to be a marker of allergic reaction. However, the present authors' study revealed the serum from severely ill rheumatoid patients contained a lot of this factor.
Present study is aimed to clear the relationship between the joint destruction with the IgE receptor using immuno-histochemical procedure.
The IgE receptor is expressed on the synovial surface lining cell line and at the deep layr of the rheumatoid granulation. This factor is localized mainly in the cell matrix, and partially on the cell wall.
IgE receptor contained cell were distributed around the rheumatoid joint destruction and surrounded by the many mast cells which include the granules for the acute allergic reaction.
The present authors suggest that IgE receptor is to be a marker and/or inducing factor of joint destruction.

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Published: 1995-03-27  

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