Staphylococcus aureus NAD kinase promotes infection by protecting bacteria from host antimicrobial defenses and by supporting production of major virulence factors.

The pathogenic success of Mycobacterium tuberculosis relies in part on its ability to blunt a component of the TLR2-dependent immune response.

The sickle cell trait strongly protects against not only retinopathy-positive cerebral malaria but also retinopathy-negative cerebral malaria, providing evidence that malarial parasites also contribute to retinopathy-negative cerebral malaria and are not innocent bystanders.

The first lethal Junín virus challenge model in immunocompetent mice provides insight into New World mammarenavirus pathogenesis and will serve as a model for the development of much-needed therapeutic interventions.

ESRP1 is central to intestinal barrier integrity in mice and humans and alterations in ESRP1 function or expression contribute to intestinal pathology, partly through modified expression of ESRP1-specific GPR137 isoforms.

Type-I interferon enriched microenvironment generated by Mycobacterium tuberculosis induces the Siglec-1 receptor expression in human macrophages, including on tunneling nanotubes, and contributes to the exacerbation of cell-to-cell transfer of HIV-1.

Combined evidence of human genetics, in vitro cardiomyocyte differentiation, and mouse model indicates that SORBS2 is a regulator of second heart field development and its deficiency causes seemingly opposite atrial septal defects.

Perinatal granulopoiesis and cord blood serum PGLYRP-1, a specific granule protein, are altered prior to onset of childhood asthma and provide potential targets for early identification of at-risk populations.

Transition from healthy to diseased state is a cell-type-specific process, influenced by neighboring cells and resulting in functionally meaningful differences between pulmonary artery adventitial fibroblasts and smooth muscle cells.

By binding with their type 1 pili to the cell surface receptor CD14, pathogenic E. coli suppress the capacity of dendritic cells to activate T cells.