Correlation between Autoimmune Disease Frequency and IL-2 Expression Due to Treg Cells

Abstract

In some circumstances, immune cells attack their normal cells. CD4+ helper T lymphocytes are mainly in charge of removing some lymphocytes that contain receptors with self-antigens to develop self-tolerance, and regulatory T cells (Treg) are in charge of additional potential risk. Treg cells suppress immune responses by consuming IL-2 cytokines, essential for T cell responses. IL-2 molecules activate naive CD4+ T cells into CD4+ Treg cells through the STAT5s signaling process and positive feedback of CD25 production with the FoxP3 transcription factor. Therefore, IL-2 cytokines are responsible for two opposite roles: activating immune responses through T cell proliferation and inhibiting immune responses by binding to regulatory T cells instead of proliferating T cells. Due to IL-2’s precise ability to control immune responses, IL-2 expression showed a relatively high correlation with autoimmune disease frequency compared to other interleukin substances. The IL-2 expression amount and autoimmune disease prevalence in five tissues showed a relatively high negative coefficient of determination, indicating a tissue with low IL-2 expression would have a high percentage of the autoimmune disease occurring and less likely to occur in tissue with high IL-2 expression. However, as the control of immune responses is very important, many alternative routes can substitute when one is blocked that turned up as exceptions. Nevertheless, the IL-2 expression was found to have a stronger relationship with autoimmune disease occurrence than other interleukins, except IL-10, which is a product of IL-2 functioning.