Cryptogenic abscess of the liver evidence of underlying
reticuloendothelial cell dysfunction.
On 5th day of postinfection moderate histopathological lesions observed depleted and necrosed B lymphocytes observed at medullar area of bursal lymphoid follicle, depleted lymphocytes replaced by heterophils and
reticuloendothelial cells. The immature B-cells is believed to be first site of replication for IBD virus where virus causes damage to B cells in lymphoid follicles of bursa (Chen et al., 2009).
In the liver of chronic hepatitis C (CHC) patients, iron deposition has been found in both hepatocytes and
reticuloendothelial cells [sup][9],[10],[11],[12],[13] although the mechanism is not fully clarified.
Tangier disease is a homozygous defect in ABCA1 that typically results in very low HDL-C, peripheral neuropathy, and lipid-laden
reticuloendothelial cells manifesting as characteristic enlarged orange tonsils and hepatosplenomegaly.
They are then transported intra-cellularly via the lymphatics to organs rich in
reticuloendothelial cells, and from there travel to other organs and tissues, where they can cause inflammation, granuloma formation, necrosis, and abscess formation.
While Tfr2[alpha] is involved in the hepatic pathway regulating iron hormone hepcidin (Hamp) [7], Tfr2[beta] is involved in iron efflux from
reticuloendothelial cells [8].
Intestinal iron absorption and iron recycling in
reticuloendothelial cells are coordinately orchestrated in order to maintain iron levels in the circulation adequate for the needs of the various tissues and organs but insufficient to activate dangerous ROS production [13, 14].