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Centrilobular Kupffer cells, with a grey granular cytoplasm, in a resolving liver injury. Liver biopsy. Trichrome stain.

Kupffer cells, also known as Browicz-Kupffer cells, are specialized macrophages located in the liver that form part of the reticuloendothelial system (RES) (aka: mononuclear phagocyte system).



The cells were first observed by Karl Wilhelm von Kupffer in 1876.[1] The scientist called them "sternzellen" (star cells or stellate cells) but thought, falsely, that they were an integral part of the endothelium of the liver blood vessels and that they originated from it. In 1898, after several years of research, Tadeusz Browicz, a Polish scientist, identified them, correctly, as macrophages. [2][3]


Their development begins in the bone marrow with the genesis of promonocytes and monoblasts into monocytes, and then on to peripheral blood monocytes, completing their differentiation into Kupffer cells.[4]


The red blood cell is broken down by phagocytic action, and the hemoglobin molecule is split. The globin chains are re-utilized, while the iron-containing portion or heme is further broken down into iron, which is re-utilized and bilirubin, which is conjugated with glucuronic acid within hepatocytes and secreted into the bile.

Helmy et al. identified a receptor present in Kupffer cells, the complement receptor of the immunoglobulin family (CRIg). Mice without CRIg could not clear complement system-coated pathogens. CRIg is conserved in mice and humans and is a critical component of the innate immune system.[5]

Function in alcoholic liver disease

Kupffer cells activation are responsible for early ethanol-induced liver injury, common in chronic alcoholics. Chronic alcoholism and liver injury deal with a two hit system. The second hit is characterized by an activation of the Toll-like receptor 4 (TLR4) and CD14, receptors on the Kupffer cell that internalize endotoxin (LPS). This activates the transcription of pro-inflammatory cytokines (Tumor necrosis factor-alpha) and production of superoxides (a pro-oxidant). TNFα will then enter the stellate cell in the liver, leading to collagen synthesis and fibrosis. Fibrosis will eventually cause cirrhosis, or loss of function of the liver.[6]


  1. ^ Haubrich WS. Kupffer of Kupffer cells. Gastroenterology 2004;127:16. PMID 15236167.
  2. ^ Szymanska R, Schmidt-Pospula M. Studies of liver's reticuloendothelial cells by Tadeusz Browicz and Karl Kupffer. A historical outline. Arch Hist Med (Warsz). 1979;42(3):331-6. PMID 386989.
  3. ^ Stachura J, Galazka K. History and current status of Polish gastroenterological pathology. J Physiol Pharmacol. 2003 Dec;54 Suppl 3:183-92. PMID 15075472.
  4. ^ Naito M, Hasegawa G, Takahashi K. Development, differentiation, and maturation of Kupffer cells. Microsc Res Tech 1997;39:350-64. PMID 9407545.
  5. ^ Helmy K, Katschke K, Gorgani N, Kljavin N, Elliott J, Diehl L, Scales S, Ghilardi N, van Lookeren Campagne M (2006). "CRIg: a macrophage complement receptor required for phagocytosis of circulating pathogens". Cell 124 (5): 915–27. doi:10.1016/j.cell.2005.12.039. PMID 16530040.  
  6. ^ Michael D. Wheeler, Ph.D. (2004). "Endotoxin and Kupffer Cell Activation in Alcoholic Liver Disease.". National Institute on Alcohol Abuse and Alcoholism of the NIH.  

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