Abstract
Background: Systemic lupus erythematosus (SLE) is an autoimmune disease which may be caused by development of the autoantibodies. On the other hand, SLE is a high-risk group of atherosclerosis, so it is possible that some of autoantibodies in SLE are the result of atherosclerosis-related diseases such as cerebral infarction (CI), cardiovascular disease (CVD) and diabetes mellitus (DM). Methods: The initial screening of autoantibodies was performed using the protein array method. AlphaLISA was used to analyze the serum antibody levels using synthetic polypeptides as antigens. Results: After the initial screening using protein array, we identified 67 antigens that were recognized by IgG antibodies in sera of patients with SLE. In the second screening, 170 peptides derived from amino acid sequences of 67 antigens were synthesized and used as antigens for analysis of serum antibody levels by AlphaLISA. The antibody levels for ten peptides were significantly higher in the sera of patients with SLE than in those of healthy donors. Further AlphaLISA analysis of sera of patients with CI, CVD or DM revealed that the serum antibody levels for four peptides derived from SOSTDC1, CTNND1, CLDND1 and CCNG2 were elevated in patients as compared to those of healthy donors. Conclusions: Serum antibody levels against peptide antigens of SOSTDC1, CTNND1, CLDND1 and CCNG2 are useful markers for diagnosis of the progression of CI, CVD and/or DM.
Highlights
Systemic lupus erythematosus (SLE) is a chronic inflammatory disorder characterized by damage to multiple organ systems caused by the production of many autoantibodies, generation of immune complexes, and activation of the complement system [1,2,3]
Initial screening of SLE-specific antigens by protein array By using protein microarrays loading with 9,480 proteins, we examined 6 sera from SLE patients and 5 sera from healthy controls to identify SLE-associated antigens
Sixty-seven proteins such as SOSTDC1, CTNND1 were selected as antigens by reacting with more than 5 sera from SLE patients and not with any of the sera from healthy donors (Table 1)
Summary
Systemic lupus erythematosus (SLE) is a chronic inflammatory disorder characterized by damage to multiple organ systems caused by the production of many autoantibodies, generation of immune complexes, and activation of the complement system [1,2,3]. Dysfunction of T cells and accelerated activation of B cells in SLE patients [4] enables the development of various autoantigens such as the anti-nuclear antibody [5]. In the study of large case series of patients with SLE, 6-20% and 4-15% of deaths were due to cardiovascular disease (CVD) and cerebrovascular disease, respectively [12,13,14]. To estimate the onset risk of accelerated atherosclerosis in SLE patients, several markers have been introduced including C-reactive protein [15], lipoprotein (a) [16], homocysteine [17], inflammatory cytokines [18,19], yet the satisfactory results have not been obtained. Systemic lupus erythematosus (SLE) is an autoimmune disease which may be caused by development of the autoantibodies. SLE is a high-risk group of atherosclerosis, so it is possible that some of autoantibodies in SLE are the result of atherosclerosis-related diseases such as cerebral infarction (CI), cardiovascular disease (CVD) and diabetes mellitus (DM)
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