The Fgl2/fibroleukin prothrombinase contributes to immunologically mediated thrombosis in experimental and human viral hepatitis
J. Clin. Invest. Philip A. Marsden, et al. 112:58 doi:10.1172/JCI18114 [Go to this article.]

Figure 4
Fibrin deposition and cellular necrosis in livers of Fgl2/fibroleukin–deficient mice following MHV-3 infection. (a) Liver from C57Bl/6 (susceptible) mouse 3 days after infection. We note widespread confluent fibrin deposition and necrosis involving greater than 90% of liver tissue. (b) Liver from A/J (resistant) mouse. Liver tissue is normal with no fibrin deposition or necrosis. (c) Liver from Fgl2/fibroleukin^+/+ mouse. We noted that the liver shows confluent fibrin deposition and necrosis. (d) Liver from Fgl2/fibroleukin^+/– mouse. Fibrin deposition and necrosis and scattered foci are seen. (e) Liver from Fgl2/fibroleukin^–/– mouse. We noted that the livers were essentially free of fibrin deposition and necrosis. Only small, rare foci of fibrin deposition and necrosis were evident.