Proteomic surveillance of autoimmunity in OA: identification of TPI as an autoantigen in patients with OA

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Arthritis Rheum. 2004 May;50(5):1511-21.

Proteomic surveillance of autoimmunity in osteoarthritis: identification

of triosephosphate isomerase as an autoantigen in patients with

osteoarthritis.

Xiang Y, Sekine T, Nakamura H, Imajoh-Ohmi S, Fukuda H, Nishioka K, Kato

T.

Division of Immunoregulation, Department of Bioregulation, Institute of

Medical Science, St. nna University School of Medicine, 2-16-1

Sugao, Miyamae-ku, Kawasaki, Kanagawa 216-8512, Japan.

OBJECTIVE: Autoimmunity to proteins, such as type II collagen and

cartilage intermediate layer protein, that are produced by chondrocytes

has been reported in patients with osteoarthritis (OA) as well as in

patients with rheumatoid arthritis (RA). However, it remains to be

determined whether the overall specificities of the autoimmunity differ

between OA and RA patients. This study sought to clarify the differences

by applying proteomic surveillance for the detection of autoantigens

comprehensively. METHODS: Serum samples were obtained from 20 patients

with OA, 20 patients with RA, and 20 healthy volunteers. Human

chondrocyte proteins were separated from the sera by 2-dimensional

electrophoresis, and antigenic protein spots were detected by Western

blotting. The antigenic proteins were then identified by mass

fingerprinting. The antigenicity of the identified proteins was

confirmed and the prevalence of the autoantibodies in the OA, RA, and

other disease groups was determined with the use of recombinant

proteins. In addition, autoepitopes were mapped on the antigens.

RESULTS: Nineteen protein spots were recognized only by the OA sera, but

not by the RA sera. One of these proteins was identified as

triosephosphate isomerase (TPI). IgG-type anti-TPI autoantibodies were

detected in 24.7% of the serum samples and 24.1% of the synovial fluid

samples from the patients with OA, whereas <6% of the RA and systemic

lupus erythematosus samples were positive for anti-TPI. In addition,

multiple autoepitopes were identified on TPI.

CONCLUSION: The overall profile of autoimmunity in OA differs from that

in RA, which may reflect the OA-specific pathologic role of

autoimmunity. The autoantibody to TPI, detected predominantly in the OA

samples and produced by the antigen-driven mechanism, has the potential

to be used as a diagnostic marker for OA.

PMID: 15146421

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