Background Pregnancy is a state of natural immunomodulation during which most patients with rheumatoid arthritis (RA) experience spontaneous improvement of their disease. In our previous studies, genes of the innate immune cells were shown to be up-regulated during pregnancy (1). Important players of the innate immune response are type 1 interferons (IFN) (2).
Objectives To investigate whether type I IFN inducible gene signatures are modified during pregnancy in patients with RA.
Methods Peripheral blood mononuclear cells (PBMC) of patients with RA and healthy women who were recruited during and after pregnancy were evaluated for type I IFN inducible genes by GeneChip analysis. Candidate genes were further investigated by quantitative real-time PCR (qPCR) in pregnant and non-pregnant RA patients and healthy women. The influence of pregnancy serum on the expression of the pre-selected type I IFN candidate genes was measured upon stimulation with IFN-alpha or IFN-beta.
Results GeneChip analysis showed an up-regulation of most type I IFN inducible genes during the third trimester in both healthy controls as well as in RA patients. In pregnant RA patients, the gene expression of IFI35, IFI44, IFI44L, IFIT3, OAS1 and SICLEC1 peaked at the second trimester and decreased postpartum. Moreover, pregnant RA patients showed significantly higher levels of IFI44 and SICLEC as compared to pregnant healthy women. Pregnancy serum was able to induce IFI44L and IFIT3 in PBMC of non-pregnant RA patients. This effect could be increased by the addition of IFN-alpha.
Conclusions Pregnancy and RA give rise to an increased expression of type I IFN inducible genes reflecting an up-regulation of the innate immune system by both conditions.
Häupl T, Østensen M, Grützkau A, Radbruch A, Burmester GR, Villiger PM. Reactivation of rheumatoid arthritis after pregnancy: increased phagocyte and recurring lymphocyte gene activity. Arthritis Rheum. 2008;58(10):2981-92.
Van Holten J, Plater-Zyberk C, Tak PP. Interferon-beta for treatment of rheumatoid arthritis. Arthritis Res 2002;4:346-52
Disclosure of Interest None Declared
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