Th1-type immune responses by Toll-like receptor 4 signaling are required for the development of myocarditis in mice with BCG-induced myocarditis

Serum inflammatory cytokines, complement components, and soluble interleukin 2 receptor in primary biliary cirrhosis

“…This result itself is not surprising considering the relationships of inflammatory mediators in a variety of human and autoimmune murine diseases [40][41][42][43]. Indeed, that is the basis for targeted therapies [44].…”

Suppressor of Cytokine Signaling 1 DNA Administration Inhibits Inflammatory and Pathogenic Responses in Autoimmune Myocarditis

“…We previously reported that Tlr4 mutant C3H/HeJ mice are resistant to development of EAM (45). Furthermore, IL-1 type 1 receptor signaling on DCs is critical for autoimmune myocarditis development (11).…”

Biomarkers of Heart Failure in Myocarditis and Dilated Cardiomyopathy

“…In a mouse model of CVB3 myocarditis, our laboratory found that TLR4 deficient mice develop reduced acute inflammation and lower IL-1 and IL-18 levels in the heart (Fairweather et al, 2003). The importance of TLR4 signaling in a strictly autoimmune model of myocarditis was demonstrated by Nishikubo et al where TLR4 signaling was found to be necessary to mount a Th1-type immune response (Nishikubo et al, 2007). We have shown that TLR4 is upregulated on macrophages and mast cells during the innate immune response to CVB3 and during acute CVB3 myocarditis and this response results in increased inflammation and progression to DCM and HF in males compared to females (Frisancho-Kiss et al, 2007;Onyimba et al, 2011).…”

“…Evidence exists that both cellular and auto/antibodymediated damage contribute to the progression to DCM and HF following myocarditis (Cooper, 2009;Fairweather et al, 2008;Kallwellis-Opara et al, 2007). Similar to atherosclerosis, acute myocardial inflammation is associated with an elevated Th1 response in males (Daniels et al, 2008;Frisancho-Kiss et al, 2007;Huber and Pfaeffle, 1994;Nishikubo et al, 2007). A Th17 response has been shown to increase fibrosis leading to DCM in the experimental autoimmune myocarditis (EAM) model in mice (Baldeviano et al, 2010).…”