Adaptive immune response during hepatitis C virus infection

Figure 3 Scheme showing the hepatitis C virus strategies to escape from hepatitis C virus-specific cytotoxic T cells control. Hepatitis C virus (HCV) modulates the balance between positive and negative co-stimulatory molecules, between pro- and anti-apoptotic molecules, and between Th and Treg cells and develops escape mutations at TCR recognition site. PD-1: Programmed cell death protein 1; CTLA-4: Cytotoxic T-lymphocyte antigen 4; BTLA: B- and T-lymphocyte attenuator; Tim-3: T-cell immunoglobulin domain and mucin domain 3; ICOS: Inducible T-cell Costimulator; GITR: Glucocorticoid induced tumor necrosis factor receptor family related gene; Bim: Bcl-2-interacting mediator; Mcl-1: Myeloid leukemia cell differentiation protein; (-) inhibition; (+) induction.