Megan M. Eva

TL;DR: It is found that deficiency in signaling via type I interferon receptor led to deregulated activation of group 2 innate lymphoid cells (ILC2 cells) and infection-associated type 2 immunopathology.

TL;DR: It is demonstrated that regulation of type I IFN signaling is the predominant mechanism affecting the susceptibility of Usp18Ity9 mice to Salmonella infection and that hyperactivation of signaling leads to increased IL-10, deregulation of autophagic markers and increased proinflammatory cytokine production.

TL;DR: An in vivo genome-wide mutagenesis screen revealed an uncharacterized role of CYRI (FAM49B) in conferring host resistance to Salmonella infection and outlined an intricate host–pathogen signalling interplay that is crucial for determining bacterial fate.

TL;DR: The strategies and tools used in mouse genetics to understand immunity to infection with special emphasis on chemical mutagenesis of the mouse germ-line are described together with current strategies to efficiently identify functional mutations using next generation sequencing.

TL;DR: The utility of the Collaborative Cross to identify new host genetic variants controlling susceptibility to infections and improve the understanding of the function of the Itgal gene are emphasized.