Circulating human primed innate lymphoid cell precursors have the potential to functionally induce adhesion molecules' expression in endothelial cells and possibly support the immune cells' infiltration into the tumor site.
COVID-19 will have an ongoing impact on antimicrobial resistance acquisition, transmission, and burden, requiring the close attention of researchers globally to generate a complete evidence base for the shifted dynamics.
For many bacterial species, recombination dominates genome evolution and phylogenetic patterns that have so far been assumed to reflect clonal relationships, in fact reflect variation in recombination rates across lineages.
A single dose of a characterized motility-deficient mutant was sufficient to induce robust anti-protein antibodies' response and cross-protective immunity against death and colonization in two different animal models of leptospirosis.
In this ideal example of pharmacogenomics, individuals with a common variant in a gene encoding for an inflammatory lipid mediator benefit selectively from standard-of-care anti-inflammatory treatment used for tuberculous meningitis.
In the injured sciatic nerve, blood-derived monocytes and macrophages eat dying leukocytes, thereby contributing to nerve debridement and inflammation resolution, and this correlates with neuronal regeneration.
Time-lapse imaging and the modular recreation of host physiology reveal that alveolar epithelial cells, potential permissive infection sites for Mycobacterium tuberculosis, can restrict early bacterial growth via surfactant secretion.
Applying bioorthogonal chemistry to the zebrafish/Mycobacterium marinum model of tuberculosis reveals that the virulence lipid PDIM must spread into epithelial cells in order for mycobacteria to establish infection.