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Abstract Number: 2200

IgE Autoantibodies Against SSA and SSB in Patients with Sjögren’s Syndrome and Healthy Controls

Stamatina Danielides1, Barbara Dema2, Juan Rivera2 and Gabor G. Illei3, 1Nidcr, NIH, Bethesda, MD, 2Laboratory of Molecular Immunogenetics, NIAMS, NIH, Bethesda, MD, 3Sjogren's Clinic, NIDCR/ NIH, Bethesda, MD

Meeting: 2012 ACR/ARHP Annual Meeting

Keywords: Sjogren's syndrome and autoantibodies

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Session Information

Title: Sjögren's Syndrome - Clinical

Session Type: Abstract Submissions (ACR)

Background/Purpose:

Sjögren’s syndrome (SS) is a chronic autoimmune disorder, presenting as an autoimmune exocrinopathy. Although the pathogenesis of this disease is largely unknown, evidence indicates that B cells, and hence the T helper 2 environment, may play an important role in its development. Recent evidence supports that IgE double stranded DNA (dsDNA) autoantibodies may be involved in the amplification loop of T helper 2 cells in lupus. In addition, there is a correlation between the presence of IgE autoantibodies and disease activity, measured by low complement levels. We sought to determine whether autoreactive IgE autoantibodies can be found in patients with Sjögren’s syndrome.

Methods:

We included 180 patients with the diagnosis of Sjögren’s syndrome based on the American European consensus group criteria and 53 blood bank donors. We performed ELISA to determine the levels of IgG and IgE antibodies against SSA, SSB, dsDNA and Sm-RNP. Subjects with autoantibody levels over the mean +2SD of the controls were considered autoantibody positive. Statistical analysis was done with the Wilcoxon test.

Results:

IgE autoantibodies against SSA and SSB were found in higher titers and higher frequencies in SS patients compared to blood bank donors (SSA 33.8% vs 6.81%, SSB 41.67% vs 1.85% in patients vs controls respectively, p<0.0001 for both), IgE autoantibodies to Sm-RNP and albeit less frequently anti-dsDNA were also seen more commonly in SS patients than controls (Sm RNP 25% vs 1.85%, p<0.0001 and dsDNA 15.70 vs 5.55%, p=0.0156).

The presence of IgE autoantibodies was not exclusive to the group of patients with positive IgG autoantibodies, as 29.2% of patients were discordant for SSA and 26.25% for SSB IgG and IgE antibodies. 

The difference between IgG and IgE antibodies was striking for antiSm-RNP, as 7.25% of SS patients had IgG Sm-RNP and 25% had IgE Sm-RNP positivity.

No correlation was seen between IgE antibody titers and serum IgE levels or the respective IgG antibodies.

Among IgG antibodies only SSA IgG was associated with low complement levels, however several IgE autoantibodies were associated with low complements (low C3 and SSB IgE, p=0.0107; low C4 and SSB IgE p=0.0023; low C4 and SSA IgE, p=0.0316, low C4 and dsDNA IgE, p=0.0078).

There was no association between SSA or SSB IgE and focus scores.

Conclusion:

IgE autoantibodies are present in a high proportion of SS patients compared to controls, and they appear independent from their respective IgG autoantibodies. Preliminary data suggest that IgE autoantibodies may be associated with hypocomplementemia, but further studies are needed to clarify their role in the cascade of events leading to disease pathogenesis.


Disclosure:

S. Danielides,
None;

B. Dema,
None;

J. Rivera,
None;

G. G. Illei,
None.

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