Non-genetic Causes of Th17/Treg Imbalance and its Impact on Systematic Autoimmune Diseases

Abstract

Autoimmune is the situation that immune system loses self-tolerance and attacks tissues, causing inflammatory responses. Th17/Treg imbalance is the case that quantity or efficacy of pro-inflammatory helper T cell Th17 is greater than suppressive regulatory T cell, which widely observed in autoimmune diseases. Research on Th17/Treg imbalance initialized from discovering similarity between Th17 and Treg development and activation of their critical transcriptional regulator RORγt and Foxp3. In decades of studies, researchers have successfully identified risk factors and possible reasons inducing Th17/Treg imbalance, including infection, diet, environment and gut microbiota etc. Moreover, several trials of treatment based on knowledge of Th17/Treg imbalance have been successful. However, though several explanations leading to imbalance have risen, detailed signalling pathways and protein mechanisms have remained unknown due to complexity of experimental proof. This review summarizes current researching progress on understanding how Th17 and Treg matures and compares their similarity in differentiation. Moreover, this review explains the role of Th17 and Treg in immune system, and analyzes the detrimental result and reasons for Th17/Treg imbalance, using some systematic autoimmune diseases as examples. Research in Th17/Treg explains why systematic autoimmune diseases and other types of hypersensitivity can prolong excluding genetic deficiency, and discovers optimal targets to ameliorate symptoms. Future studies should explain in detail mechanism which external factors can cause imbalance and why imbalance still generates albeit sufficient conditions for Treg differentiation possess.