Laurel L. Lenz

Identification of a second Listeria secA gene associated with protein secretion and the rough phenotype.

SecA2-dependent secretion of autolytic enzymes promotes Listeria monocytogenes pathogenesis.

Promiscuity of MHC class Ib-restricted T cell responses.

TRAIL-R as a negative regulator of innate immune cell responses.

Cytosolic expression of SecA2 is a prerequisite for long-term protective immunity.

Expression of the p60 autolysin enhances NK cell activation and is required for listeria monocytogenes expansion in IFN-gamma-responsive mice.

Activation of cytosolic phospholipase A2alpha in resident peritoneal macrophages by Listeria monocytogenes involves listeriolysin O and TLR2.

Silencing the alarm: insights into the interaction between host and pathogen. Conference on Microbial Pathogenesis: Mechanisms of Infectious Disease.

Stable integration vector for nutrient broth-based selection of attenuated Listeria monocytogenes strains with recombinant antigen expression.

CD5 sweetens lymphocyte responses.

Bacterial peptidoglycan degrading enzymes and their impact on host muropeptide detection.

Induction of IFN-alphabeta enables Listeria monocytogenes to suppress macrophage activation by IFN-gamma.

Activation of naive NK cells in response to Listeria monocytogenes requires IL-18 and contact with infected dendritic cells.

Cellular reactive oxygen species inhibit MPYS induction of IFNβ.

Antagonistic crosstalk between type I and II interferons and increased host susceptibility to bacterial infections.

IL-15 and type I interferon are required for activation of tumoricidal NK cells by virus-infected dendritic cells.

Transient Receptor Potential Melastatin 2 (TRPM2) ion channel is required for innate immunity against Listeria monocytogenes.

MPYS is required for IFN response factor 3 activation and type I IFN production in the response of cultured phagocytes to bacterial second messengers cyclic-di-AMP and cyclic-di-GMP.

A LysM and SH3-domain containing region of the Listeria monocytogenes p60 protein stimulates accessory cells to promote activation of host NK cells.