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In mice, cyclic di-GMP is an effective mucosal pneumococcal vaccine adjuvant that stimulates the immune response via two distinct mechanisms.

The number of different peptides presented by major histocompatibility complex class I molecules to the immune system's T lymphocytes is inversely correlated with cell surface expression and is strongly associated with the response to infectious disease.

By contributing to the maintenance of ROS homeostasis, CD33-related Siglecs control oxidative damage and influence rate of aging and lifespan.

A novel mouse model of immunization against Plasmodium chabaudi involving infectious mosquito bites and drug-treatment elicits protection against blood-stage malaria parasites, and shows that protection is not necessarily life cycle stage-specific.

The cytotoxicity exerted by CD8⁺ T cells against parasitized erythroblasts helps to protect against blood-stage malaria by making parasitized cells susceptible to phagocytosis.

Building on previous work (St John et al., 2013), we explain why secondary infection by dengue virus is associated with more severe vascular disease than primary infection.

T cell receptor signaling is regulated by newly polymerized F-actin foci at the immunological synapse.

Differentiation of CD4 T cells into CD4 T follicular helper cells during viral infection in mice is promoted by tumor growth factor beta.

Peptide immunotherapy in mice depends upon sustained expression of co-inhibitory protein PD-1 in T cells.

HOIL-1 deficiency in mice results in a severe immunodeficiency that is effectively complemented by chronic infection with a murine gamma-herpesvirus.