1992 Fiscal Year Final Research Report Summary
Role of anti-Type II collagen antibody formation in pathogenesis of rheumatoid arthritis.
| Project/Area Number |
03670715
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Orthopaedic surgery
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| Research Institution | Jikei University School of Medicine |
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Principal Investigator |
FUJII Katsuyuki Jikei university School of Medicine Department of Orthopedics Associate professor, 医学部・整形外科, 助教授 (10112856)
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| Co-Investigator(Kenkyū-buntansha) |
MARUMO Keishi Jikei University School of Medicine Department of Orthopaedics Assistant profess, 医学部・整形外科, 講師 (70199925)
SAI Shigaku Jikei University School of Medicine Department of Orthopaedics Assistant profess, 医学部・整形外科, 講師 (80183359)
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| Project Period (FY) |
1991 – 1992
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| Keywords | rheumatoid arhtritis / Type II collagen / anti-Type II collagen antibodies / autoimmunity |
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| Research Abstract |
In order to clarity the role of autoimmunity to collagen in the pathogenesis of rheumatoid arthritis(RA), we have developed an improved enzyme-linked immunosorbent assay (ELISA) for anti-collagen antibodies to diminish non-specific background interference and provide higher sensitivity. Based on this assay system, it was found that anti-collagen antibodies in RA patients are specific to Type II collagen and have no cross-reactivity with Type I and Type III collagens. The major antigenic determinants which are recognized by RA sera were found to reside in the region represented by cyanogen bromide peptide (CB) 11and CB-8 of human Type II collagen molecule. The result indicate that anti-collagen antibodies in RA patients are derived from the conformational determinants of Type II collagen molecule. Also, anti-Type II collagen antibodies were found in the articular cartilage of RA patients,and are most likely to contribute to the pathogenesis of joint destruction. Thus, the present study strongly indicate that the formation of anti-collagen anti-bodies in RA may not be the consequence of the destruction of the connective tissues. Although the stimulus for the development of autoimmunity to native Type II colagen RA remains unknown, the immunization seems to be functionally active at the onset and to play an important role for chronic perpetuation of the disease.
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Research Products
(6 results)
