In contrast, IL-20−/− mice exhibited reduced levels of alanine aminotransferase and aspartate aminotransferase as well as hepatic necrosis and increased levels of IL-6 after Concanavalin A administration compared to WT mice, suggesting that IL-20−/− mice are resistant to Concanavalin A-induced hepatitis and are associated with selective upregulation of IL-6 with hepatoprotective properties. Here, IL6 is linked to hepatitis A virus infection.