Protein biomarkers of inflammation in women with SLE and their newborn children.

OBJECTIVES

In utero exposure to maternal anti-Ro/Sjögren's syndrome antigen A (SSA) and anti-La/Sjögren's syndrome antigen B (SSB) autoantibodies activates the fetal type I interferon (IFN) system. Women with SLE often carry a broader range of autoantibodies beyond anti-Ro/SSA and anti-La/SSB, like for example, anti-double stranded DNA (anti-dsDNA), anti-centromere and anti-nucleosome antibodies. We aimed to assess IFN activation and the expression of other immune-related proteins in pregnant women with SLE-with or without anti-SSA/SSB or anti-dsDNA autoantibodies-and in their newborns. We also aimed to investigate the impact of maternal immunomodulatory treatment on these responses.

METHODS

Serum samples from 22 women with SLE and 22 healthy pregnant women, along with their newborns, were analysed using proximity extension assay technology to quantify 92 immune-related proteins.

FINDINGS: Women with SLE had differential expression of 39 out of 92 proteins compared with healthy controls. Several proinflammatory cytokines and proteins involved in SLE pathogenesis were significantly upregulated in both women and their newborns. A couple of IFN-regulated proteins were significantly increased in anti-SSA/SSB-positive and anti-dsDNA-positive mother-child pairs, respectively. Still, IFN scores were generally elevated in pregnant women with SLE regardless of their autoantibody status. However, neonatal IFN scores did not significantly differ based on maternal autoantibody status or treatment.

CONCLUSION

Women with SLE and their newborn children had increased expression of a range of proinflammatory biomarkers irrespective of their anti-SSA/SSB or anti-dsDNA autoantibody status. Irrespective of the increased expression of several IFN-regulated proteins in anti-SSA/SSB-positive and anti-dsDNA-positive mother-child pairs, the presence of these autoantibodies alone did not significantly influence the level of IFN activation in neither the mothers nor the newborns exposed to these autoantibodies in utero.