Role of Toll-Like Receptors and Th Responses in Viral Myocarditis

Abstract

Myocarditis is the common cause of sudden cardiac death, dilated cardiomyopathy (DCM) and heart failure (HF) in young adults. The most common type of myocarditis is viral myocarditis (VMC). Toll-like receptors (TLRs) are vital to identify pathogens in vivo. TLRs promote the differentiation of naive CD4+T cells to T helper (Th) cells, activate the immune response, and participate in the pathogenesis of autoimmune and allergic diseases. Although the pathogenesis of VMC is unclear, autoimmune responses have been confirmed to play a significant role; hence, it could be inferred that VMC is closely related to TLRs and Th responses. Some drugs have been found to improve the prognosis of VMC by regulating the immune response through activated TLRs. In this review, we discuss the role of TLRs and Th responses in VMC.

Exploring the pathogenesis and immune infiltration in dilated cardiomyopathy complicated with atrial fibrillation by bioinformatics analysis

“…Inflammation and immune response are significant pathogenesis of DCM and AF ( 1 , 16 ). In the pathogenesis of viral myocarditis, the Th2 immune response induces ventricular remodeling and promotes the progression of myocarditis to DCM and heart failure, whereas the Th1 response alleviates viral myocarditis but increases acute myocardial inflammation by inhibiting Th2 responses ( 17 ). Th17 cells increase tissue inflammation and promote autoimmune activation by secreting large amounts of proinflammatory cytokines, while Treg cells can inhibit the body’s immune response and active tolerance to self-antigens through intercellular contact and secretion of inhibitory cytokines in various immune cell subsets, so as to avoid the occurrence of autoimmune diseases ( 18 ).…”