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Intrahepatic MxA expression is correlated with interferon‐alpha expression in chronic and fulminant hepatitis
Author(s) -
Leifeld Ludger,
Ramakers Jan,
Maria Schneiders Angelika,
Ludwig Dumoulin Franz,
Sterneck Martina,
Müller Andreas,
Sauerbruch Tilman,
Spengler Ulrich
Publication year - 2001
Publication title -
the journal of pathology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.964
H-Index - 184
eISSN - 1096-9896
pISSN - 0022-3417
DOI - 10.1002/path.903
Subject(s) - fulminant hepatic failure , alpha (finance) , alpha interferon , interferon , immunohistochemistry , kupffer cell , cytokine , medicine , immunology , biology , liver transplantation , construct validity , transplantation , nursing , patient satisfaction
Interferon‐alpha (IFN‐α) has potent pro‐inflammatory and anti‐viral functions. It exerts its effects by inducing intracellular proteins such as MxA. To analyse the role of intrahepatic interferon activation, IFN‐α and MxA expression was studied by immunohistochemistry in explant livers of 20 patients with fulminant hepatic failure (FHF), 41 patients with chronic liver disease (CLD), and ten normal controls (NCs). In NCs only small numbers of Kupffer cells, but no hepatocytes, showed IFN‐α and MxA expression. In contrast, significantly enhanced numbers of IFN‐α‐ and MxA‐positive Kupffer cells, along with small numbers of MxA‐positive and larger numbers of IFN‐α‐positive lymphocytes, were found in CLD and in FHF. MxA protein was also expressed on hepatocytes and bile ducts in the vicinity of IFN‐α‐positive inflammatory infiltrates (hepatocytes: NCs: 0%, CLD: 8%, FHF: 68%; bile ducts: NCs: 19%, CLD: 46%, FHF: 83%). A significant correlation was found between the numbers of IFN‐α‐ and MxA‐positive cells ( r =0.67, p <0.001). Thus, large amounts of IFN‐α are released in the livers of patients with FHF, which is likely to contribute to immune‐mediated liver cell damage. Intrahepatic MxA expression corresponds to IFN‐α produced particularly by infiltrating inflammatory cells, rather than by hepatocytes themselves. Copyright © 2001 John Wiley & Sons, Ltd.