LIGHT Induces Distinct Signals to Clear an AAV-Expressed Persistent Antigen in the Mouse Liver and to Induce Liver Inflammation

Background: Infection with adeno-associated virus (AAV) vector with liver tropism leads to persistent expression of foreign antigens in the mouse liver, with no significant liver inflammation or pathology. This provides a model to investigate antigen persistence in the liver and strategies to modulate host immunity to reduce or clear the foreign antigen expressed from AAV vector in the liver. Methods/Principal Findings: We showed that expressing LIGHT with an adenovirus vector (Ad) in mice with established AAV in the liver led to clearance of the AAV. Ad-LIGHT enhanced CD8 effector T cells in the liver, correlated with liver inflammation. LTbR-Ig proteins blocked Ad-LIGHT in clearing AAV. Interestingly, in LTbR-null mice, Ad-LIGHT still cleared AAV but caused no significant liver inflammation. Conclusions/Significance: Our data suggest that LIGHT interaction with the LTbR plays a critical role in liver inflammation but is not required for LIGHT-mediated AAV clearance. These findings will shed light on developing novel immunotherapeutic

Chromoblastomycosis as an endemic disease in temperate Europe: first confirmed case and review of the literature

This study reports a case of a 56-year-old white male, retired coal-miner, diagnosed with chromoblastomycosis lasting 20 years. The infection site was the burnt skin of the back. For many years the patient had not undertaken any treatment believing that the lesion had been a burn scar. A gradual increase in lesion size prompted the patient to start therapy. The diagnosis was made by histopathological examination and mycological culture. Identification of the causative agent at the species level was achieved by sequence analysis of the internal transcribed spacer (ITS) region and D1/D2 domains of the 26S rDNA. To our knowledge, this is the first documented case of chromoblastomycosis caused by Fonsecaea monophora in temperate Europe, outside the endemic area for the disease. This finding is highly significant for understanding the routes of infection of chromoblastomycosis and radically revises the traditional view of the natural ecology of the etiological agents of the disease