How pregnancy can affect autoimmune diseases progression?

Abstract

Autoimmune disorders are characterized by tissue damage, caused by self-reactivity of different effectors mechanisms of the immune system, namely antibodies and T cells. Their occurrence may be associated with genetic and/or environmental predisposition and to some extent, have implications for fertility and obstetrics. The relationship between autoimmunity and reproduction is bidirectional. This review only addresses the impact of pregnancy on autoimmune diseases and not the influence of autoimmunity on pregnancy development. Th17/Th1-type cells are aggressive and pathogenic in many autoimmune disorders and inflammatory diseases. The immunology of pregnancy underlies the role of Th2-type cytokines to maintain the tolerance of the mother towards the fetal semi-allograft. Non-specific factors, including hormonal changes, favor a switch to Th2-type cytokine profile. In pregnancy Th2, Th17/Th2 and Treg cells accumulate in the decidua but may also be present in the mother’s circulation and can regulate autoimmune responses influencing the progression of autoimmune diseases.

Risks associated with viral infections during pregnancy

“…It is well established that the immunological changes associated with pregnancy can result in the amelioration of some autoimmune disorders, such as multiple sclerosis or rheumatoid arthritis (95), but can also increase the severity of several types of viral infections. For example, pregnant women have higher mortality rates associated with varicella virus infection, which is 10 times more likely to be complicated by pneumonia during pregnancy (94,96,97).…”

Maternal plasma proteomics in a rat model of pregnancy complications reveals immune and pro‐coagulant gene pathway activation

“…IPA was performed using the proteomics assay's findings (Table 1) healthy pregnancy in mammals. 33,34 Therefore, LEW rats could model women with a predisposition to Th1 disease. [10][11][12][13][14][15][16] It is well shown that maternal immune maladaptation is a key observation in multiple pregnancy disorders including recurrent miscarriage, preterm birth, intrauterine growth restriction, and pre-eclampsia.…”

Associations of maternal oestradiol, cortisol, and TGF‐β1 plasma concentrations with thyroid autoantibodies during pregnancy and postpartum

“…During pregnancy, there is a shift from Th1/Th17 to Th2 immunity. Thus, Th1/Th17‐associated autoimmune diseases remit during pregnancy while they flare‐up in postpartum …”

“…Increased oestradiol concentrations during pregnancy enhance Th2 responses . Oestrogens induce the decrease of IL‐17 production in experimental allergic encephalomyelitis while they inhibit Th17 differentiation and disease progression via oestrogen receptor α (ERα) in T cells . Cortisol favours the Th1 to Th2 shift resulting thus, to decrease of Th1‐related autoimmune phenomena, while it has a direct positive effect on Th2 cells by up‐regulating the production of the Th2‐associated cytokines IL‐4, IL‐10, and IL‐13 .…”

“…Thus, Th1/Th17-associated autoimmune diseases remit during pregnancy while they flare-up in postpartum. 9 Oestradiol concentrations in maternal serum rise steadily from the first trimester of pregnancy until term and decline rapidly in the postpartum period. 10 Cortisol, the end-product of the hypothalamicpituitary-adrenal (HPA) axis, is steadily increased during pregnancy.…”