1. Autoimmune Hepatitis After Liver Transplantation
Rodrigo Liberal, Maria Serena Longhi, Charlotte R. Grant, Giorgina Mieli–Vergani, Diego Vergani 
Clinical Gastroenterology and Hepatology 
Volume 10, Issue 4, Pages (April 2012)
DOI: /j.cgh
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2. Figure 1
De novo AIH. The portal tract is densely infiltrated by mononuclear cells, with a clear presence of plasma cells, that invade the parenchyma, disrupting the limiting plate (Picture provided by Dr Yoh Zen, Institute of Liver Studies, King's College Hospital).
Clinical Gastroenterology and Hepatology  , DOI: ( /j.cgh )
Copyright © 2012 AGA Institute Terms and Conditions

3. Figure 2
In recurrent AIH, the recipient's immune system is sensitized to species-specific antigens and has a pool of memory cells that are restimulated and re-expanded after presentation of antigens (or autoantigens) by the recipient's APCs, which repopulate the grafted liver. In rejection, the targets are primarily MHC molecules or minor histocompatibility antigens. APCs that promote rejection are of either donor or recipient origin; whereas the former are present in the graft as passenger leukocytes that cause direct activation of the recipient's T cells, the latter are located in draining lymphoid tissues, acquiring antigens that are shed from the allograft and presenting them to the recipient's T cells, causing their indirect activation.
Clinical Gastroenterology and Hepatology  , DOI: ( /j.cgh )
Copyright © 2012 AGA Institute Terms and Conditions

4. Figure 3
Bone marrow–derived T-cell precursors enter the thymus and are eliminated if their affinity for self is either too high or too low. Cells with an intermediate affinity for self are permitted into the periphery, where they are controlled by thymus-derived regulatory (Treg) cells. After liver transplantation, the release of self-antigens from the liver cell or an infection with microorganisms that are structurally similar to self activates quiescent autoreactive T cells. This process is facilitated by the administration of calcineurin inhibitors (CNI) such as cyclosporine and tacrolimus, which would promote efflux of self-reactive precursors from the thymus and impair the function of Treg cells.
Clinical Gastroenterology and Hepatology  , DOI: ( /j.cgh )
Copyright © 2012 AGA Institute Terms and Conditions