Abstract
A successful pregnancy requires the maternal immune system to accept a fetus expressing allogeneic paternal antigens and provide competent responses to infections. Accordingly, maternal-fetal immune abnormalities may have an important role in the development of recurrent spontaneous abortion (RSA). Ever since the establishment of the association between immunologic abnormalities and RSA, various types of immune therapy to restore normal immune homeostasis have been increasingly developed. Although previous studies have focused on the maternal-fetal interface, non-invasive examination is of great importance in clinical practice. The present study investigated the balance between type-17 T-helper (Th17) and T-regulatory (Treg) cells in the peripheral blood to improve the current understanding of the pathogenesis of RSA. Imbalances in Th17/Treg cells and associated molecular profiles were observed in patients with RSA. Furthermore, it was determined that the immunosuppressant cyclosporine A reduced the proportion of Th17 cells and promoted Treg-cell dominance by upregulating the expression of co-inhibitory molecules in pregnant females with a history of RSA. Progesterone, the traditional maternal-care drug, also had a certain immunomodulatory role through restoring the levels of several co-inhibitory molecules (including T-cell immunoglobulin mucin family member-3, programmed cell death-1 and cytotoxic T-lymphocyte associated protein-4) in the treatment of RSA. Changes in these immune molecules within the maternal peripheral blood may be indicators for monitoring pregnancy and prediction of RSA.