[37] Outcome of Patients Transplanted for Primary Sclerosing Cholangitis - Analysis of the European Liver Transplant Registry

Schramm, Christoph; Bubenheim, Michael; O’Grady, Joseph P.; Buckels, J.; Pollard, S.; Neuhaus, P.; Jamieson, Neville V.; Klempnauer, J.; Rogiers, Xavier; Karam, V.; Adam, René; Lohse, Ansgar W.

doi:10.1016/s0168-8278(07)61635-3

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“…In a clinical scenario in human AIH, our data imply that anti-TNF-α may be a new therapeutic option to prevent recurrence for patients undergoing liver transplantation for AIH, who have a high potential its recurrence [28,29]. However, the use of anti-TNF-α for patients with initial presentation of AIH may be limited to cases of mild to moderate severity or AIH before progression to fulminant hepatic failure.…”

Section: Discussionmentioning

confidence: 91%

TNF-α is essential in the induction of fatal autoimmune hepatitis in mice through upregulation of hepatic CCL20 expression

Iwamoto

Kido

Aoki

et al. 2013

Clinical Immunology

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It is unclear what roles TNF-α has in the development of autoimmune hepatitis (AIH) and whether AIH is responsive to anti-TNF-α. We recently developed a mouse model of fatal AIH that develops in PD-1-deficient mice thymectomized three days after birth, finding that CCR6-CCL20 axis-dependent migration of dysregulated splenic T cells is crucial to induce AIH. In this study, we show the indispensable role of TNF-α in the development of AIH. Administering anti-TNF-α prevented the induction, but treatment by anti-TNF-α after the induction did not suppress progression. Administering anti-TNF-α did not prevent splenic T-cell activation, but did suppress hepatic CCL20 expression. In contrast, administering anti-CCL20 suppressed AIH but not elevated serum TNF-α levels. TNF-α stimulation enhanced CCL20 expression in hepatocytes. These findings suggest that TNF-α is essential in the induction of AIH through upregulation of hepatic CCL20 expression, which allows migration of dysregulated splenic T cells.

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Section: Discussionmentioning

confidence: 91%