The complete removal of a pulmonary hydatid cyst by bronchoscopy occurs rarely in clinical practice. We describe a 22-year-old male originally from Lebanon, with suspected hydatid cyst rupture on computed tomography chest after experiencing sudden onset fevers and cough whilst taking empiric anthelmintic therapy. Bronchoscopy revealed white gelatinous material in the posterior segment of the left lower lobe.
View Article and Find Full Text PDFObjective: Nonsteroidal antiinflammatory drugs (NSAID) are used as first-line agents to treat acute gout. Recent trials suggest a possible first-line role for corticosteroids.
Methods: We conducted a metaanalysis of randomized controlled trials (RCT) evaluating corticosteroid versus NSAID therapy (nonselective and selective) as treatment for acute gout.
Crucial to Natural Killer T (NKT) cell function is the interaction between their T-cell receptor (TCR) and CD1d-antigen complex. However, the diversity of the NKT cell repertoire and the ensuing interactions with CD1d-antigen remain unclear. We describe an atypical population of CD1d-α-galactosylceramide (α-GalCer)-reactive human NKT cells that differ markedly from the prototypical TRAV10-TRAJ18-TRBV25-1(+) type I NKT cell repertoire.
View Article and Find Full Text PDFαβ and γδ T cells are disparate T cell lineages that can respond to distinct antigens (Ags) via the use of the αβ and γδ T cell Ag receptors (TCRs), respectively. Here we characterize a population of human T cells, which we term δ/αβ T cells, expressing TCRs comprised of a TCR-δ variable gene (Vδ1) fused to joining α and constant α domains, paired with an array of TCR-β chains. We demonstrate that these cells, which represent ∼50% of all Vδ1(+) human T cells, can recognize peptide- and lipid-based Ags presented by human leukocyte antigen (HLA) and CD1d, respectively.
View Article and Find Full Text PDFThe T cell repertoire comprises αβ and γδ T cell lineages. Although it is established how αβ T cell antigen receptors (TCRs) interact with antigen presented by antigen-presenting molecules, this is unknown for γδ TCRs. We describe a population of human Vδ1(+) γδ T cells that exhibit autoreactivity to CD1d and provide a molecular basis for how a γδ TCR binds CD1d-α-galactosylceramide (α-GalCer).
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