Regulation of Inflammation in Autoimmune Disease

Inflammation is a normal physiological defense against pathogen infection and tissue damage and quickly ends under normal circumstances.However, in many chronic conditions, the inflammatory response continues and leads to significant tissue and organ damage.Recently, increasing evidences have shown that the abnormal inflammatory response is closely associated with many chronic diseases, especially in autoimmune diseases, including rheumatoid arthritis (RA), inflammatory bowel disease (IBD), systemic lupus erythematosus (SLE), gout, and diabetes [1][2][3].Although the importance of inflammatory dysregulation in chronic illnesses has been reported in recent studies, the pathogenesis of inflammation dysfunction in the autoimmune diseases remains elusive.Knowledge of the mechanism of inflammation regulation will lead to significant clinical benefits for the treatment of autoimmune disease.This special issue showcases a number of original research articles and review papers on the topic of inflammatory regulation in autoimmune diseases.T cell-mediated inflammatory responses have long been recognized to play an essential role in the development of autoimmune diseases, including Th1, Th2, and Th17 cell responses.Recent compelling evidence has shown that abnormal T cell immune response, including Th1, Th2, and Th17 cell responses, was actually having a crucial role in the inflammation of autoimmune diseases [4].Recent studies showed that vasoactive intestinal peptide (VIP) modulates the pathogenic activity of diverse cell subpopulations involved in RA, including lymphocytes, fibroblast-like synoviocytes (FLS), and macrophages [5].In this special issue, R. Villanueva-Romero