Regular ArticleEffect of Interleukin-18 on Viral Myocarditis: Enhancement of Interferon- γ and Natural Killer Cell Activity☆
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Innate and adaptive immunity in acute myocarditis
2024, International Journal of CardiologyNatural killer cells in inflammatory heart disease
2017, Clinical ImmunologyCitation Excerpt :The ability of NK cells to limit viral infections is important in cardiac biology [105–108]. NK cells are required for protection against mouse models of CBV and MCMV-mediated myocarditis in an IFNγ-dependent manner [90,109,110]. Clinically, rare individuals with NK cell deficiencies have an increased susceptibility to viral infections, though not specifically cardiac infections [111–114].
Viral Infection and Heart Disease: Autoimmune Mechanisms
2015, Infection and AutoimmunityRegulatory effects of IL-18 on cytokine profiles and development of myocarditis during Trypanosoma cruzi infection
2014, Microbes and InfectionCitation Excerpt :In fact, there is an intense inflammatory response in the heart, which is differently modulated and dependent on the parasite strain [6,23,24]. IL-18 is a proinflammatory cytokine induced during T. cruzi infection in mice [3,19] and humans [25] which also induces the production of IFN-γ [11–15] and other pro-inflammatory cytokines including IL-1β and TNF-α [26]. However, to this date, the role of IL-18 in T. cruzi infection has remained unclear.
Inflammation in viral myocarditis: Friend or foe?
2012, Trends in Molecular MedicineCitation Excerpt :Dose and time dependency were also observed for IL-6, as transgenic overexpression of IL-6 aggravates the course of EMCV myocarditis [51], whereas recombinant IL-6 administration in the acute, but not subacute, phase is protective [52]. Similarly, beneficial effects of IL-18 treatment (involving enhanced NK cell activity) were only observed from treatment at the time of infection, whereas initiation of treatment at day 2 post-infection failed to provide cardioprotection [53]. Detrimental roles have been ascribed to two other proinflammatory cytokines, IL-1 and IL-12.
Cardiac Cell-specific Apoptotic and Cytokine Responses to Reovirus Infection: Determinants of Myocarditic Phenotype
2009, Journal of Cardiac FailureCitation Excerpt :IL-10 treatment in an EMCV mouse model resulted in increased survival, decreased myocardial lesions and decreased levels of TNF-α, but had no effect on myocardial virus concentration.56 IL-18 has been demonstrated to have similar beneficial attributes: increased survival, decreased viral titer, decreased myocardial necrosis, increased IFN- γ expression in the heart, and increased natural killer cell activity in the spleen.57 Specific to reovirus associated myocarditis, Sherry et al have identified IFN-β and the resulting cascade of effects as important factors in the control of viral replication.39,42,58,59
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Please address all correspondence to: Tsugiyasu Kanda, MD, Department of Laboratory Medicine, Gunma University School of Medicine, 3-39-15, Showa-machi, Maebashi 371, Japan. Fax: +81 272 20 7720. E-mail: [email protected]