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Study reveals why pregnancy often improves rheumatoid arthritis

Type I interferon (IFN) may help explain why some women with rheumatoid arthritis (RA) show an improvement during pregnancy

Type I interferon (IFN) may help explain why some women with rheumatoid arthritis (RA) show an improvement during pregnancy, according to a study published in the journal Arthritis Research & Therapy and led by Dr. Damini Jawaheer of the University of California.

RA is a common systemic inflammatory disease that primarily affects joints. Its etiopathogenesis remains elusive, although studies have established that both genetic and environmental factors play a role. Current clinical treatments of RA still have drawbacks, such as high doses, frequent administration, and serious side effects.

Interestingly, published literature shows that pregnancy is associated with a remarkable change in RA severity. During pregnancy, the majority of female patients with RA display a natural improvement in their disease, while others either show no change or show a deterioration. What causes these differences remains to be answered.

In this work, researchers from University of California, University of Washington, Aarhus University, and University of Copenhagen teamed up to address this question. They mainly focused on gene expression changes induced by pregnancy in women with RA. In total, 11 women RA and 5 healthy women were enrolled in the study. Their gene expression profiles before pregnancy and at the third trimester were obtained by using RNA sequencing technique. Eight of the 11 women with RA experienced an improvement in disease at the third trimester, while the other three women worsened.

Comparing gene expression of the participants, the researchers found that the majority of pregnancy-induced changes seen in women with RA were also seen in healthy women. Importantly, they identified a small cluster of genes that showed opposite behaviors in women with RA improved and women with RA worsened during pregnancy, and all these genes were inducible by type I IFN. In women with RA improved, these IFN-inducible genes were up-regulated at the third trimester in comparison with before pregnancy, suggesting that type I IFN appears to play a beneficial role in RA.

In conclusion, the study supports a potential role of type I IFN in the natural improvement of RA during pregnancy, though more research is needed to better elucidate the expression of the IFN-inducible genes in RA during pregnancy and their impacts on the regulation of RA severity.