Spleen and liver

Abstract

In liver cirrhosis, the spleen is a source of nitric oxide which affects a hyperdynamic state typical of portal hypertension. It is generally accepted that pancytopenia results predominantly from the increased phagocytosis and destruction of hemocytes in splenic macrophages. In addition, liver fibrosis is amplified by migrated Th2 lymphocytes and transforming growth factor beta from the spleen. There is a possibility that increase of the spleen stiffness is the primary factor of idiopathic portal hypertension. Spleen stiffness is caused by bleeding, fibrosis, and calcareous deposits after increase in red pulp pressure due to venous congestion. In nonalcoholic steatohepatitis, macrophage activity in the spleen is upregulated. In addition, high levels of inflammatory cytokines are produced and T cell shows increased proliferation in the spleen. In autoimmune hepatitis model, CD4+ T cells are differentiated into follicular helper T cells (TFH) in the spleen. TFH cells promoted hypergammaglobulinemia and antinuclear antibodies production. TFH cells migrate from the spleen to the liver, triggering induction of autoimmune hepatitis in this model. IgM-positive B cells localize in the CD21-positive lymph follicle in the spleen of primary biliary cholangitis. These findings prove that the spleen influences on the pathogenesis and severity of several kinds of liver disease.