4.2. Th17 cells in myocarditis
Myocarditis is an inflammatory heart disease that can develop into a fatal cardiomyopathy[46,47]. Acute immune activation during myocarditis occurs with an autoimmune response to myosin heavy chain 6 (MYH6)[48]. Subsequent chronic stimulation of the MYH6-specific Th cells, Th1 and Th17 cells, produced inflammatory cardiomyopathy[49]. More than 30 viruses are known to cause VMC. The most common are group B (coxsackievirus B, CVB), CVA and adenovirus. Initial studies suggest that CD4 + T cells in VMC bodies are increased and differentiated towards Th1, secrete IFN-γ to reduce viral replication, thus reducing infiltration and inflammatory stimulation of myocardial immune cells, protecting against excessive immune damage and reducing the degree of myocardial fibrosis[50]. Furthermore, the type Th2 cellular immune response can reduce acute myocarditis by regulating T cells and anti-inflammatory cytokines.The immune response of Th2 cells made mice progress from myocarditis to dilated cardiomyopathy. In contrast, the Th17 cell response has increased during acute and chronic myocarditis, and was found to be involved in cardiac remodelling and dilated cardiomyopathy[51]. Th17 cells play a critical role in the development of myocarditis and dilated cardiomyopathy along with the generation of anti-myocardial antibodies in patients who are suffer from viral myocarditis. Relevant studies have shown that the serum IL-17 levels in patients with acute viral myocarditis, were positively associated with B-cell activity, which was found to produce anti-myocardial antibodies in the acute stageand with the help of Th17 cells, which aggravated myocardial injury. Clinical data also found a substantial increase in Th17 cells in patients with acute myocarditis[52], confirming that Th17 cells are specific for acute myocardial injury.