Dengue infection is an important tropical disease worldwide. The host immune response has been studied in order to better understand lesion mechanisms. It was performed an immunohistochemical study in 14 specimens of liver from patients with
dengue hemorrhagic fever (DHF) to characterize
cytokines and some factors present in liver lesions and their possible role in the pathogenesis of hepatic injury. Portal tract and hepatic acinus presented high expression of TLR2, TLR3,
IL6, and
granzyme B. Hepatic acinus also presented iNOS,
IL18, and
TGF-beta. Cells expressing
IL12,
IL13, JAk1, STAT1, and NF-κB were rarely visualized. Treg cells foxp3+ were absent. TLR2 and TLR3 seem to participate in cellular activation and
cytokine production. Cytotoxic response seems to play a role. Although
TGF-beta promotes the activation of Foxp3+ regulatory T cells,
IL6 can significantly suppresses their generation. The expression of Treg cells is diminished probably as a result of the high frequency of these
cytokines. Both
cytokines play a role in the increased vascular permeability and
edema observed in
dengue liver specimens, with consequent plasma leakage and severity of the disease. It was observed a regular expression of
IL-18 in hepatocytes and lymphocytes of the inflammatory infiltrate in portal tract, which reflects the acute inflammatory response that occurs in the liver and contributes to hepatic injury. At least in part, the increased number of cells expressing
IL-18 could play a role of "up" regulation of FasL and correlate to the phenomenon of apoptosis, a mechanism of destruction of hepatocytes in DHF.