Unlabelled: β-Lactam hypersensitivity is the most frequently self-reported drug hypersensitivity reaction. However, most of these patients are not truly allergic. The label of B.
View Article and Find Full Text PDFObjective: Chronic Chagas Cardiomyopathy (CCC) carries a high risk of embolic events due to structural changes in the left ventricle and frequent conduction disorders. However, there is limited data on anticoagulant prescription patterns and factors influencing the use of direct oral anticoagulants (DOACs) in these patients. This study aims to characterize CCC patients based on the anticoagulant therapy received and identify factors associated with DOACs use.
View Article and Find Full Text PDFInborn errors of immunity are monogenic disorders that predispose patients to immune dysregulation, autoimmunity, and infection. Some autoimmune diseases, such as autoimmune cytopenias, systemic lupus erythematosus, and inflammatory bowel diseases, are increasingly recognized as phenotypes of inborn errors of immunity. The objective of this article was to identify red flags or clinical/laboratory markers to suspect inborn errors of immunity in patients with autoimmune cytopenias, systemic lupus erythematosus, and inflammatory bowel diseases through a systematic literature review.
View Article and Find Full Text PDFThe aim of this work is to evaluate different molecular strategies deployed by indigenous isolates of Trichoderma in their interaction with the phytopathogen Botrytis cinerea. In vitro antagonism assays, determination of volatile and diffusible compounds, and the relative expression of the prb1 gene, which codes for an extracellular protease, before and during the stage of direct contact between the two fungi, were carried out; the characterization of this protease was also performed. All 17 Trichoderma strains tested showed high levels of inhibition against B.
View Article and Find Full Text PDFTertiary lymphoid structures (TLSs) are de novo ectopic lymphoid aggregates that regulate immunity in chronically inflamed tissues, including tumours. Although TLSs form due to inflammation-triggered activation of the lymphotoxin (LT)-LTβ receptor (LTβR) pathway, the inflammatory signals and cells that induce TLSs remain incompletely identified. Here we show that interleukin-33 (IL-33), the alarmin released by inflamed tissues, induces TLSs.
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