Figure 2.
Anatomy of the hepatic sinusoid. The hepatic sinusoids are lined by a population of microvascular LSECs that separate hepatocytes and stellate cells from leukocytes circulating through the liver in the blood. Fenestrations in the LSEC lining allow the passive exchange of molecules between the space of Dissé and the blood, as well as direct contact of lymphocyte filopodia with hepatocyte microvilli. The liver interstitium is highly enriched in cells of the innate immune system (such as antigen-presenting dendritic, Kupffer, natural killer, and NKT cells [not shown]) and in T cells, which participate in adaptive immune responses. Mediators produced by both parenchymal and nonparenchymal cells, including IL-10, TGFβ, arginase, and PGE2, regulate immune function within the liver. LSEC, liver sinusoidal endothelial cells; TGFβ, transforming growth factor-β. Reprinted from Thomson et al91 with permission.

Anatomy of the hepatic sinusoid. The hepatic sinusoids are lined by a population of microvascular LSECs that separate hepatocytes and stellate cells from leukocytes circulating through the liver in the blood. Fenestrations in the LSEC lining allow the passive exchange of molecules between the space of Dissé and the blood, as well as direct contact of lymphocyte filopodia with hepatocyte microvilli. The liver interstitium is highly enriched in cells of the innate immune system (such as antigen-presenting dendritic, Kupffer, natural killer, and NKT cells [not shown]) and in T cells, which participate in adaptive immune responses. Mediators produced by both parenchymal and nonparenchymal cells, including IL-10, TGFβ, arginase, and PGE2, regulate immune function within the liver. LSEC, liver sinusoidal endothelial cells; TGFβ, transforming growth factor-β. Reprinted from Thomson et al91  with permission.

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