Diana S. Hansen

Regulation of murine cerebral malaria pathogenesis by CD1d-restricted NKT cells and the natural killer complex.

The lack of suppressor of cytokine signalling-1 (SOCS1) protects mice from the development of cerebral malaria caused by Plasmodium berghei ANKA.

CD1d-restricted NKT cells contribute to malarial splenomegaly and enhance parasite-specific antibody responses.

Regulation of immunity and pathogenesis in infectious diseases by CD1d-restricted NKT cells.

Transcriptional profiling reveals suppressed erythropoiesis, up-regulated glycolysis, and interferon-associated responses in murine malaria.

The natural killer complex regulates severe malarial pathogenesis and influences acquired immune responses to Plasmodium berghei ANKA.

Severe malarial anemia of low parasite burden in rodent models results from accelerated clearance of uninfected erythrocytes.

CD4+ CD25+ regulatory T cells suppress CD4+ T-cell function and inhibit the development of Plasmodium berghei-specific TH1 responses involved in cerebral malaria pathogenesis.

NK cells stimulate recruitment of CXCR3+ T cells to the brain during Plasmodium berghei-mediated cerebral malaria.

gammadelta-T cells expressing NK receptors predominate over NK cells and conventional T cells in the innate IFN-gamma response to Plasmodium falciparum malaria.

The role of leukocytes bearing Natural Killer Complex receptors and Killer Immunoglobulin-like Receptors in the immunology of malaria.

Putative IKDCs are functionally and developmentally similar to natural killer cells, but not to dendritic cells.

Plasmodium falciparum erythrocyte membrane protein-1 specifically suppresses early production of host interferon-gamma.

CXCR3 determines strain susceptibility to murine cerebral malaria by mediating T lymphocyte migration toward IFN-gamma-induced chemokines.

Blood-stage Plasmodium infection induces CD8+ T lymphocytes to parasite-expressed antigens, largely regulated by CD8alpha+ dendritic cells.

IP-10-mediated T cell homing promotes cerebral inflammation over splenic immunity to malaria infection.

Murine cerebral malaria: the whole story.

Natural regulatory T cells in malaria: host or parasite allies?

NK cells and conventional dendritic cells engage in reciprocal activation for the induction of inflammatory responses during Plasmodium berghei ANKA infection.

Advances in infection and immunity: from bench to bedside.