The IL-33/ST2 pathway controls coxsackievirus B5-induced experimental pancreatitis

• Published in: The Journal of immunology (1950) Vol. 191; no. 1; pp. 283 - 292
• Main Authors: Sesti-Costa, Renata, Silva, Grace K, Proença-Módena, José L, Carlos, Daniela, Silva, Maria L, Alves-Filho, José C, Arruda, Eurico, Liew, Foo Y, Silva, João S
• Format: Journal Article
• Language: English
• Published: United States 01.07.2013
• Subjects: Animals; Cells, Cultured; Coxsackievirus; Coxsackievirus Infections - immunology; Coxsackievirus Infections - metabolism; Coxsackievirus Infections - pathology; Disease Models, Animal; Interleukin-1 Receptor-Like 1 Protein; Interleukin-33; Interleukins - administration & dosage; Interleukins - biosynthesis; Interleukins - physiology; Mice; Mice, Inbred BALB C; Mice, Knockout; Pancreatitis - immunology; Pancreatitis - pathology; Pancreatitis - virology; Receptors, Interleukin - biosynthesis; Receptors, Interleukin - physiology; Signal Transduction - immunology; Viral Load - immunology; Weight Loss - immunology

Coxsackievirus B (CVB) is a common cause of acute and chronic infectious myocarditis and pancreatitis. Th1 cells producing IFN-γ and TNF-α are important for CVB clearance, but they are also associated with the pathogenesis of inflammatory lesions, suggesting that the modulation of Th1 and Th2 balanc...