Abstract
BackgroundSjögren’s syndrome (SS) is a primary autoimmune disease (pSS) or secondarily associated with other autoimmune diseases (sSS). The mechanisms underlying immune dysregulation in this syndrome remain unknown, and clinically it is difficult to diagnose owing to a lack of specific biomarkers.MethodsWe extracted immunoglobulins (Igs) from the sera of patients with sSS associated with rheumatoid arthritis (RA) and used them to screen a phage display library of peptides with random sequences.ResultsOur results show that an sSS-specific peptide, designated 3S-P, was recognized by sera of 68.2% (60 of 88) patients with sSS, 66.2% of patients with RA-sSS, and 76.5% of patients with systemic lupus erythematosus (SLE)-sSS. The anti-3S-P antibody was scarcely found in patients with pSS (1.8%), RA (1.3%), SLE (4.2%), ankylosing spondylitis (0%), and gout (3.3%), as well as in healthy donors (2%). The 3S-P-binding Igs (antibodies) were used to identify antigens from salivary glands and synovial tissues from patients with sSS. A putative target autoantigen expressed in the synovium and salivary gland recognized by anti-3S-P antibody was identified as self-vimentin.ConclusionsThis novel autoantibody is highly specific in the diagnosis of sSS, and the underlying molecular mechanism of the disease might be epitope spreading involved with vimentin.
Highlights
Sjögren’s syndrome (SS) is a primary autoimmune disease or secondarily associated with other autoimmune diseases
Phage clones with the sequence YSLHNAGPWSLQ bound to the IgGs of patients with rheumatoid arthritis (RA)-secondarily associated with other autoimmune diseases (sSS), which was confirmed by three rounds of screening with the same pooled IgGs
Further investigation revealed that this peptide was recognized by sera of 68.2% (60 of 88) patients with sSS (66.2% of patients with RAsSS and 76.5% of patients with systemic lupus erythematosus (SLE)-sSS) (Fig. 1a)
Summary
Sjögren’s syndrome (SS) is a primary autoimmune disease (pSS) or secondarily associated with other autoimmune diseases (sSS). The mechanisms underlying immune dysregulation in this syndrome remain unknown, and clinically it is difficult to diagnose owing to a lack of specific biomarkers. Sjögren’s syndrome (SS) is a systemic autoimmune disease characterized by marked reduction of exocrine glandular secretions, and it progresses to lymphocytic infiltration and destruction of exocrine glands [1,2,3]. In addition to arising as a primary disease (primary Sjögren’s syndrome [pSS]), pSS occurs in association with other autoimmune diseases (secondary Sjögren’s syndrome [sSS]), rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE) [4,5,6,7]. The molecular mechanism of sSS is unknown, and the lack of specific biomarkers constrains efforts to establish the clinical diagnosis of and intervention for the disease.
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