The characterization of ancient B19V and HBV genotype A4 viruses circulating during Colonial epidemics provides new insights into the pathogens that were introduced to the Americas after the European colonization.
Mucosal-associated invariant T (MAIT) cells, highly activated and dysfunctional in sepsis patients, contribute to tissue-specific cytokine responses that are protective against mortality during experimental sepsis.
Single-cell RNA-sequencing identifies the precise cellular and molecular events that occur along the sepsis timeline in the kidney, pointing to potential biomarkers and therapeutic targets.
Killing their neighbors allows bacteria to steal genes, including antibiotic resistance genes, which we observed under a microscope, quantified, modeled, and predicted potentially guiding strategies to combat it.
Apoptotic cells release molecules to recruit macrophages, but do not cause inflammation because they also secrete AMP that functions as a ‘calm down’ signal.
Sepsis-induced numerical loss of naive autoantigen-specific CD4 T cells reduces host capacity to develop autoimmune immune disease, thereby demonstrating an intriguing relationship between infection and autoimmune disease.
Interbacterial interactions can promote mutagenesis, and possibly adaptation, when intoxicated cells survive exposure to type VI secretion-delivered DNA deaminase toxins.
