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.