Ursodeoxycholic acid (UDCA) has been shown by many studies to be of benefit in the treatment of primary biliary cirrhosis (PBC) and also of primary sclerosing cholangitis (PSC) (and other cholestatic liver diseases), but the mechanism of action of this drug remains obscure and is, in all probability, of multifactorial nature. Possibly, complex interaction of immunomodulatory and membrane-stabilizing effects in conjunction with an altered composition of the bile acid pool are responsible for the beneficial effect.
This book, the proceedings of Falk Symposium No. 86 `Bile Acids and Immunology' (Part 1 of the Basel Liver Week), held in Basel, Switzerland, October 17-18, 1995, starts with an update on important mechanisms involved in autoimmune mediated processes covering the presentation of antigens and autoantigens by professional and non-professional antigen presenting cells, the recognition of the MHC-antigen complex by T-cells, the role of natural and disease-specific antibodies, as well as the control of immune processes via TH1/TH2 cells and their cytokines. It then focuses on the recent findings concerning the aetiopathogenesis of PBC and PSC and the effect of UDCA therapy in these disorders.
The most relevant questions which have to be answered in this field are:
This book, the proceedings of Falk Symposium No. 86 `Bile Acids and Immunology' (Part 1 of the Basel Liver Week), held in Basel, Switzerland, October 17-18, 1995, starts with an update on important mechanisms involved in autoimmune mediated processes covering the presentation of antigens and autoantigens by professional and non-professional antigen presenting cells, the recognition of the MHC-antigen complex by T-cells, the role of natural and disease-specific antibodies, as well as the control of immune processes via TH1/TH2 cells and their cytokines. It then focuses on the recent findings concerning the aetiopathogenesis of PBC and PSC and the effect of UDCA therapy in these disorders.
The most relevant questions which have to be answered in this field are:
- Is the biochemical improvement the consequence of a true antiinflammatory or immunosuppressive effect of UDCA or only due to the replacement of hydrophobic by hydrophilic bile acids?
- Does UDCA increase the efficacy of immunosuppressive drugs and is it necessary to differentiate between patients who need either a mono-UDCA or a combined (UDCA/steroids) therapy?
- Are PBC and PSC true autoimmune disorders driven by an autoantigen or only `secondary autoimmune' processes induced by a persisting infectious agent, considering the poor response of both disorders to immunosuppressive treatment as compared to patients with autoimmune hepatitis?
