Last, some immune-mediated diseases may either be caused or activated as a result of prior pregnancies. To explain, fetal cells and free fetal DNA are detectable in maternal blood beginning early in pregnancy (Simpson, 2013; Sitar, 2005; Waldorf, 2008). Fetal cell microchimerism is the persistence of fetal cells in the maternal circulation and in organs following pregnancy. These fetal cells may become engrafted in maternal tissues and stimulate autoantibodies. This raises the possibility that fetal cell micro chimerism leads to the predilection for autoimmune disorders among women (Adams, 2004). Evidence for this includes fetal stem cells engrafted in tissues in women with autoimmune thyroiditis and systemic sclerosis Gimenez, 2005; S;ivatsa, 2001). Such microchimerism has also been described in women with SLE and those with rheumatoid arthritis-associated HLA alleles (da Silva, 2016; Lee, 2010; Rak, 2009a). Conversely, engrafted maternal cells may provoke autoimmune conditions in a woman's ofspring (Ye, 2012; Stevens, 2016).
Lupus is a heterogeneous autoimmune disease with a complex pathogenesis that results in interactions between susceptibility genes and environmental factors (Hahn, 2015). Immune system abnormalities include overactive B lymphocytes that are responsible for autoantibody production. hese result in tissue and cellular damage when autoantibodies or immune complexes are directed at one or more cellular nuclear components (T sokos, 201r1). In addition, immunosuppression is impaired, including regulatory T-cell function (Tower, 2013). Some autoantibodies produced in patients with SLE are shown in Table
Almost 90 percent of SLE cases are in women, and its prevalence in those of childbearing age approximates 1 in 500 (Lockshin, 2000). Accordingly, the disease is encountered relatively frequently during pregnancy. The 10-year survival rate is 70 to 90 percent (Tsokos, 201r1). Infection, lupus lares, endorgan failure, hypertension, stroke, and cardiovascular disease account for most deaths.
Genetic inluences are implicated by a higher concordance with monozygotic compared with dizygotic twins-25 versus 2 percent, respectively. Moreover, frequency in patients with one afected family member is 10 percent. he relative risk of disease rises if there is inheritance of the "autoimmunity gene" on chromosome 16 that predisposes to SLE, rheumatoid arthritis, Crohn disease, and psoriasis. Susceptibility genes such as HA-Al, -B8, -D3, -DBl, and -TET3 explain only a portion of the genetic heritability (Tsokos, 201r1; Yang, 2013). Interestingly, even maternal exposure to fetal genes elevates susceptibility to SLE development. A case-control study found that a child's HLA-DRB1 genotype increases the risk of SLE in the mother (Cruz, 2016). Furthermore, neonatal lupus erythematosus has been reported in an infant conceived via oocyte donor to a mother with autoimmune disease with circulating anti-Ro and anti-La antibodies (Chiou, 2016).