Chronic hepatitis C and the risk for atherosclerotic and cardiomyopathic heart disease

Table 1 Overview of the cell types, cytokines with their actions on target cells

Cytokine	T helper cell type	Target cell	Action	Net effect on plague formation
TNF-α	Th1	Macrophages, endothelial cells	Promotes atherogenesis by increasing the expression of adhesion molecules on endothelial cells, leading to the recruitment of inflammatory cells into the arterial wall	Proatherogenic
IFN-γ	Th1	Macrophages, CD8, T cells, NK cells	Despite its antiviral effects, it increases adhesion molecules expression	Proatherogenic
IL-2	Th1	T cell	B cell clonal expansion and T cell development	Proatherogenic (less well-established)
IL-4	Th2	T and B cells	Promotes T cell development, upregulate pro-inflammatory mediators	Antiatherogenic (less well-established)
IL-5	Th2	B cell	B cell activation and production of protective natural immunoglobulin M antibodies against oxidation-specific antigens	Antiatherogenic (less well-established)
IL-6	Macrophages	Macrophages, Th1	Increase adhesion molecule expression	Proatherogenic
IL-8	Th2	Neutrophils	Releasing reactive oxygen species and promoting inflammation	Proatherogenic
IL-10	T reg cell	Macrophages, B cells	Suppresses activation of Th1 cells and macrophages	Antiatherogenic

TNF-α: Tumor necrosis factor-alpha; IL: Interleukin-6; IFN-γ: Interferon-gamma; NK: Natural killer.