No abstract

The intrahepatic biliary tree shows a site-characteristic expression and induction of TFF1,2,3 and DMBT1. In large bile ducts, TFF1,3 were constitutively expressed and increased in pathologic bile ducts. In small bile ducts, TFF2/DMBT1 is induced in damaged ducts irrespective of etiologies. However, the cytoprotective/repair property of TFF2/DMBT1 may not be enough to prevent the following bile duct loss in PBC.

Epidermal γδ T cells that reside in the front line of the skin play a pivotal role in stress immune surveillance. However, it is not clear whether these cells are involved in further induction of immune responses after they are activated in dysregulated epidermis. In this study, we found that activated γδ T cells expressed occludin and migrated into draining lymph nodes in an occludin-dependent manner. Epidermal γδ T cells in occludin-deficient mice exhibited impairments in morphology changes and motility, although they expressed activation markers at levels comparable to those in wild-type cells. Occludin deficiency weakened the induction of allergen-induced contact hypersensitivity, primarily as the result of the impaired migration of epidermal γδ T cells. Thus, occludin expression by epidermal γδ T cells upon activation in response to epidermal stress allows them to move, which could be important for augmentation of immune responses via collaboration with other cells.

We report here an autopsy case of primary squamous cell carcinoma of the liver in a 63-year-old man who had hypercalcemia and an elevated serum level of parathyroid hormone-related protein. At autopsy, primary squamous cell carcinoma of the liver was found, without distinct preceding or associated hepatic or biliary diseases; no extrahepatic primary focus of squamous cell carcinoma was found. Bone involvement was not demonstrated, either radiologically or pathologically. Immunohistochemically, parathyroid hormone-related protein was detectable in the squamous cell carcinoma cells and it may have been responsible for the hypercalcemia. Such a case has not been reported so far in the English-language or the Japanese literature.

Several cases of granulomatous phlebitis of small hepatic veins are reported in the literature, though the etiology remains unclear. We experienced a similar case of granulomatous phlebitis involving terminal hepatic venules and this case will be reported in comparison with two previous cases presenting in our laboratory. A 39-year-old-female had a long course of medical treatment for epilepsy. She suffered from acute liver injury after prolonged fever for more than 1 week. Leukocytosis (11,100/ micro L) without eosinophilia, and inflammatory reactions such as C-reactive protein (21.0 mg/dL) were pointed out. She suffered from transient disseminated intravascular coagulation, but these abnormalities recovered with antibiotic and steroid therapy. Liver biopsy revealed granulomatous lesions mainly involving terminal hepatic venules. The possibility of tuberculosis was excluded by a negative Thiel-Nielsen stain and a negative molecular study for bacterial deoxyribonucleic acid of Mycobacteria species. Extrahepatic involvements were not clear clinically. This case and the previous two cases shared granulomatous phlebitis of the intrahepatic small hepatic veins, as well as clinical features suggestive of bacterial infection. Clinicians should be aware of such a rare clinicopathological entity.