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Anti-20S Proteasome Antibodies in Psoriatic Arthritis

INÉS COLMEGNA, BRUNO SAINZ Jr, GUSTAVO CITERA, JOSE A. MALDONADO-COCCO, ROBERT F. GARRY, and LUIS R. ESPINOZA

ABSTRACT.

Objective. Proteasomes are targets of humoral autoimmune response in patients with connective tissue diseases and other organ-specific autoimmune diseases. The finding of circulating proteasomes in psoriasis, the multiplicity of mechanisms regulated by proteasomes that are also implicated in the pathogenesis of psoriatic arthritis (PsA), and the increasing evidence linking PsA and autoimmunity led us to evaluate whether the 20S proteasome represents an antibody target in PsA.

Methods. Serum samples from 36 patients with PsA and 30 age- and sex-matched healthy subjects were tested for the presence of anti-20S proteasome antibodies (anti-20S antibody). Additional controls included 24 patients with systemic lupus erythematosus (SLE) and 20 with rheumatoid arthritis (RA). The associations of anti-20S antibodies with clinical, laboratory, and therapeutic measures were evaluated.

Results. 27.8% of the PsA patients were positive for anti-20S antibody compared to 41.6% of the SLE group and 5% of the RA group. None of the healthy subjects were seropositive for anti-20S antibody. In PsA, anti-20S seropositivity was not associated with the presence of other autoantibodies or with a particular subgroup of articular involvement.

Conclusion. Immunoreactivity against proteasomes occurs frequently in patients with PsA. This finding supports the concept of PsA as an autoimmune disease and opens new avenues for investigating its pathogenesis. (J Rheumatol First Release Feb 15 2008)

Key Indexing Terms:

PSORIATIC ARTHRITIS
PROTEASOME ANTIBODIES
IMMUNOREACTIVITY
20S PROTEASOME

From the Section of Rheumatology, Department of Medicine, Louisiana State University Health Sciences Center, New Orleans; Department of Microbiology and Immunology, Tulane University Health Sciences Center, New Orleans, Louisiana, USA; and Section of Rheumatology, IREP, University of Buenos Aires, Buenos Aires, Argentina.

I. Colmegna, MD, Post-Doctoral Fellow, Section of Rheumatology, LSUHSC-NOLA; B. Sainz Jr, PhD, Post-Doctoral Fellow, Department of Microbiology and Immunology, Tulane University HSC-NOLA; G. Citera, MD, Section of Rheumatology, IREP, University of Buenos Aires; J.A. Maldonado-Cocco, MD, Chief, Section of Rheumatology, IREP, University of Buenos Aires; R.F. Garry, PhD, Professor, Department of Microbiology and Immunology, Tulane University HSC-NOLA; L.R. Espinoza, MD, Professor, Chief, Section of Rheumatology, LSUHSC-NOLA.

Address reprint requests to Dr. L.R. Espinoza, LSU Medical Center, 1542 Tulane Ave., New Orleans, LA 70112. E-mail: luisrolan@msn.com

Accepted for publication November 14, 2007.