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a Rheumatology,
Immunology and Genetics Programme, Institute of Medical Science, St
Marianna University, School of Medicine 2-16-1, Sugao, Miyamae-ku,
Kawasaki, Kanagawa, 216-8512, Japan, b Mitsubishi Kagaku Bio-Clinical Laboratories Inc,
3-30-1, Shimura, Itabashi-ku, Tokyo, 174-8555, Japan, c Department of Orthopaedic Surgery, Okayama
University School of Medicine, 2-5-1, Shikata-cho, Okayama, 700-8558, Japan, d Department
of Biochemistry and Molecular Dentistry, Okayama University Dental
School, 2-5-1, Shikata-cho, Okayama, 700-8558, Japan
Correspondence to: Dr Kato rigplken{at}air.linkclub.or.jp
Accepted for publication 26 April 2000
OBJECTIVE
To
investigate whether autoimmunity to YKL-39, a recently cloned
cartilage protein, occurs in patients with rheumatoid arthritis (RA).
METHODSAutoantibody
to YKL-39 was assayed by enzyme linked immunosorbent assay (ELISA) and
western blotting in serum samples from patients with RA, systemic lupus
erythematosus (SLE), and healthy donors, using recombinant YKL-39
protein. This reactivity was compared with that against a YKL-39
homologue, YKL-40 (human cartilage gp-39/chondrex), which has been
reported to be an autoantigen in RA.
RESULTSAutoantibody
to YKL-39 was detected in seven of 87 patients with RA (8%), but not
in serum samples from patients with SLE or healthy donors. YKL-40
reactivity was found in only one of 87 RA serum samples (1%), with no
cross reactivity to YKL-39.
CONCLUSIONThe
existence of anti-YKL-39 antibody in a subset of patients with RA is
reported here for the first time. Further, it was shown that the immune
response to YKL-39 was independent of that to YKL-40. Clarification of
the antibody and T cell responses to autoantigens derived from
chondrocyte, cartilage, or other joint components may lead to a better
understanding of the pathophysiology of joint destruction in patients
with RA.
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