Ito cell

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Ito cells, also known as hepatic stellate cells or fat-storing cells, are pericytes found in the perisinusoidal space (a small area between the sinusoids and hepatocytes) of the liver. The stellate cell is the major cell type involved in liver fibrosis, which is the formation of scar tissue in response to liver damage.

Ito cells can be selectively stained with gold chloride, but their distinguishing feature in routine histological preparations is the presence of multiple lipid droplets in their cytoplasm. [1]

In normal liver, stellate cells are described as being in a quiescent state. Quiescent stellate cells represent 5-8% of the total number of liver cells.[2] Each cell has several long protrusions that extend from the cell body and wrap around the sinusoids. The lipid droplets in the cell body store vitamin A. The function and role of quiescent hepatic stellate cells is unclear. Recent evidence suggests a role as a liver-resident antigen-presenting cell presenting lipid antigens to and stimulating proliferation of NKT cells.[3]

When the liver is damaged, stellate cells can change into an activated state. The activated stellate cell is characterized by proliferation, contractility, and chemotaxis. The amount of stored vitamin A decreases progressively in liver injury.[1] The activated stellate cell is also responsible for secreting collagen scar tissue, which can lead to cirrhosis.

Literature

  • John P. Iredale (2001) Hepatic Stellate Cell Behavior During Resolution of Liver Injury. Seminars in Liver Disease, 21(3):427-436 PMID 11586470 - free fulltext article from Medscape.

References

  1. 1.0 1.1 Stanciu A, Cotutiu C, Amalinei C. (2002) New data about ITO cells. Rev Med Chir Soc Med Nat Iasi. 107(2):235-9. PMID 12638266
  2. Geerts A. (2001) History, heterogeneity, developmental biology, and functions of quiescent hepatic stellate cells. Semin Liver Dis. 21(3):311-35. PMID 11586463
  3. Kaufmann (2007) "Ito Cells are Liver-Resident Antigen-Presenting Cells for Activating T Cell Responses" Immunity 26, 117-129, January 2007 PMID 17239632

See also

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