Sinonasal Teratocarcinosarcoma- A Rare Tumour not so Rarely Misdiagnosed.

Sinonasal teratocarcinosarcoma (STCS) is a rare, morphologically heterogeneous and highly aggressive tumour of ambiguous origin. It is characterized by the presence of benign and malignant epithelial, mesenchymal and neuroectodermal components. Because of their rarity and heterogeneity, these lesions are often misdiagnosed, leading to management difficulties. Adequate sampling with a high index of suspicion is needed to diagnose this rare tumour. We reported here a 48-year old man with right nasoethmoidal mass eroding the cribriform plate with intracranial extension. An initial incisional biopsy was performed and a diagnosis of craniopharyngioma was made. Subtotal endoscopic excision of the mass revealed features of STCS. Immunohistochemistry confirmed the same. The patient was subsequently treated with radiotherapy. The histogenesis, histopathological features, immunohistochemistry findings, clinical features and treatment were discussed here. Till date, there are less than 100 cases reported in English literature.

Culling of activated CD4 T cells during typhoid is driven by Salmonella virulence genes.

Pathogen-specific CD4 T cells are activated within a few hours of oral Salmonella infection and are essential for protective immunity. However, CD4 T cells do not participate in bacterial clearance until several weeks after infection, suggesting that Salmonella can inhibit or evade CD4 T cells that are activated at early time points. Here, we describe the progressive culling of initially activated CD4 T cells in Salmonella-infected mice. Loss of activated CD4 T cells was independent of early instructional programming, T cell precursor frequency, and Ag availability. In contrast, apoptosis of Ag-specific CD4 T cells was actively induced by live bacteria in a process that required Salmonella pathogenicity island-2 and correlated with increased expression of PD-L1. These data demonstrate efficient culling of initially activated Ag-specific CD4 cells by a microbial pathogen and document a novel strategy for bacterial immune evasion.

Salmonella flagellin induces bystander activation of splenic dendritic cells and hinders bacterial replication in vivo.

Bacterial flagellin is a target of innate and adaptive immune responses during Salmonella infection. Intravenous injection of Salmonella flagellin into C57BL/6 mice induced rapid IL-6 production and increased expression of activation markers by splenic dendritic cells. CD11b(+), CD8alpha(+), and plasmacytoid dendritic cells each increased expression of CD86 and CD40 in response to flagellin stimulation, although CD11b(+) dendritic cells were more sensitive than the other subsets. In addition, flagellin caused the rapid redistribution of dendritic cells from the red pulp and marginal zone of the spleen into the T cell area of the white pulp. Purified splenic dendritic cells did not respond directly to flagellin, indicating that flagellin-mediated activation of splenic dendritic cells occurs via bystander activation. IL-6 production, increased expression of activation markers, and dendritic cell redistribution in the spleen were dependent on MyD88 expression by bone marrow-derived cells. Avoiding this innate immune response to flagellin is important for bacterial survival, because Salmonella-overexpressing recombinant flagellin was highly attenuated in vivo. These data indicate that flagellin-mediated activation of dendritic cells is rapid, mediated by bystander activation, and highly deleterious to bacterial survival.