Article
Anti-beta-adrenoceptor autoantibodies are elevated in systemic sclerosis
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Published: | October 8, 2019 |
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Background: G protein-coupled receptors (GPCR) are expressed by many cells, including leukocytes. Apart from natural ligands, there are circulating anti-GPCR autoantibodies which are thought to modulate functions of GPCR. We hypothesise that GPCR expressed by immune cells interact with circulating anti-GPCR autoantibodies, leading for instance to modulation of the cytokine profile.
Methods: Serum samples were received from patients suffering from systemic sclerosis (SSc, n=16), rheumatoid arthritis (RA, n=15) and giant cell arteritis (GCA, n=15) as well as from age- and sex-matched healthy controls (HC, n=15). IgG fractions were isolated from six sera out of each group using protein G affinity chromatography. Afterwards, concentrations of eight anti-GPCR autoantibodies were measured both in serum and IgG fractions using ELISA. Cytokine concentrations were measured by flow cytometry in serum using a commercial bead-based immunoassay.
Results: IgG-purification did not change the anti-GPCR antibody profile. Autoantibodies directed against beta1- and beta2-adrenoceptors were increased in both, serum (p<0.01) and IgG (p<0.05) derived from SSc patients compared to RA, GCA and HC. Concentrations of interleukin 6 in serum were increased in SSc as well as in RA and GCA compared to HC (p<0.05). In contrast, the amount of interleukin 4 in serum derived from GCA patients was higher than in SSc (p<0.05). No correlations were observed between the anti-beta-adrenoceptor autoantibody concentrations and the cytokine profile in sera.
Conclusion: Anti-beta-adrenoceptor autoantibodies are increased in serum of SSc and this pattern is maintained in purified IgG. To detect assumed alterations in the cytokine profile, direct interactions between anti-GPCR IgG autoantibodies and immune cells may be required.