Signet-ring cell/histiocytoid carcinoma of the eyelid: a case report and review of the literature.

Signet-ring cell/histiocytoid carcinomas of the eyelid are rare, slow-growing, and locally aggressive tumors. They predominantly affect elderly men and clinically resemble chronic inflammatory process such as blepharitis and chalazion. To date, the histogenesis of the tumors is still controversial. Only 27 cases of primary signet-ring cell/histiocytoid carcinomas of the eyelid are published in the literature. Local recurrence and distant metastasis occur in 8 and 7 cases, respectively. We report clinical, radiographic, and pathological features of a case of signet-ring cell/histiocytoid carcinoma of the eyelid with review of relevant literature.

Antiviral immune responses in H5N1-infected human lung tissue and possible mechanisms underlying the hyperproduction of interferon-inducible protein IP-10.

Information on the immune response against H5N1 within the lung is lacking. Here we describe the sustained antiviral immune responses, as indicated by the expression of MxA protein and IFN-alpha mRNA, in autopsy lung tissue from an H5N1-infected patient. H5N1 infection of primary bronchial/tracheal epithelial cells and lung microvascular endothelial cells induced IP-10, and also up-regulated the retinoic acid-inducible gene-I (RIG-I). Down-regulation of RIG-I gene expression decreased IP-10 response. Co-culturing of H5N1-infected pulmonary cells with TNF-alpha led to synergistically enhanced production of IP-10. In the absence of viral infection, TNF-alpha and IFN-alpha also synergistically enhanced IP-10 response. Methylprednisolone showed only a partial inhibitory effect on this chemokine response. Our findings strongly suggest that both the H5N1 virus and the locally produced antiviral cytokines; IFN-alpha and TNF-alpha may have an important role in inducing IP-10 hyperresponse, leading to inflammatory damage in infected lung.