Pregnancy represents a state of immune tolerance to avoid the rejection of the fetus. During this physiological transitory state, there have been associations with temporary remission of several autoimmune disorders, including multiple sclerosis. The fluctuations of pregnancy hormones are the hallmarks in gestation and the proper levels of the different pregnancy hormones can ensure successful implantation and fetal development. Human chorionic gonadotropin (hCG) is the first pregnancy hormones released upon conception and exploited by pregnancy tests. Here we provided a possible explanation to elucidate the phenomenon of improvements in autoimmunity during gestation. We believe that hCG is the driving factor behind the increased immune tolerance. This pregnancy hormone has potent immunosuppressive effects on T cells such as the inhibition of IL-2, impairment of cell proliferation and failure to upregulate cell activation markers. At high levels, hCG can induce cell death in T cell and B cells. With these findings, we hope that it can have the potential to be used as immunotherapy for treatment of autoimmune diseases such as multiple sclerosis

IFN-β is widely used in the treatment of multiple sclerosis, yet the mechanism facilitating its efficacy remains unclear. IL-2 production by activated T cells, including those mediating autoimmunity, and subsequent autocrine stimulation is vital for T cell expansion and function. In this study, we demonstrate that in mouse and human T cells, IFN-β specifically inhibits the production of IL-2 upon TCR engagement without affecting other cytokines or activation markers. Rather than disrupting TCR signaling, IFN-β alters histone modifications in the IL-2 promoter to retain the locus in an inaccessible configuration. This in turn is mediated through the upregulation of the transcriptional suppressor CREM by IFN-β and consequent recruitment of histone deacetylases to the IL-2 promoter. In accordance, ablation of CREM expression or inhibition of histone deacetylases activity eliminates the suppressive effects of IFN-β on IL-2 production. Collectively, these findings provide a molecular basis by which IFN-β limits T cell responses.