Lena Serghides

CD36 deficiency induced by antiretroviral therapy.

Mechanism of protection induced by vitamin A in falciparum malaria.

CD36-mediated nonopsonic phagocytosis of erythrocytes infected with stage I and IIA gametocytes of Plasmodium falciparum.

Innate immunity to malaria caused by Plasmodium falciparum.

CD36 and malaria: friends or foes?

Effect of HIV-1 antiretroviral drugs on cytoadherence and phagocytic clearance of Plasmodium falciparum-parasitised erythrocytes.

CD36 mediates the phagocytosis of Plasmodium falciparum-infected erythrocytes by rodent macrophages.

Peroxisome proliferator-activated receptor gamma and retinoid X receptor agonists have minimal effects on the interaction of endothelial cells with Plasmodium falciparum-infected erythrocytes.

Nonopsonic phagocytosis of erythrocytes infected with ring-stage Plasmodium falciparum.

Evaluation of OX40 ligand as a costimulator of human antiviral memory CD8 T cell responses: comparison with B7.1 and 4-1BBL.

Placental chondroitin sulfate A-binding malarial isolates evade innate phagocytic clearance.

Approaches to studying costimulation of human antiviral T cell responses: prospects for immunotherapeutic vaccines.

Disruption of JNK2 decreases the cytokine response to Plasmodium falciparum glycosylphosphatidylinositol in vitro and confers protection in a cerebral malaria model.

Disruption of CD36 impairs cytokine response to Plasmodium falciparum glycosylphosphatidylinositol and confers susceptibility to severe and fatal malaria in vivo.

HIV impairs opsonic phagocytic clearance of pregnancy-associated malaria parasites.

Pyruvate kinase deficiency and malaria.

C5 deficiency and C5a or C5aR blockade protects against cerebral malaria.

C5a enhances dysregulated inflammatory and angiogenic responses to malaria in vitro: potential implications for placental malaria.

Rosiglitazone modulates the innate immune response to Plasmodium falciparum infection and improves outcome in experimental cerebral malaria.

Use of peroxisome proliferator-activated receptor gamma agonists as adjunctive treatment for Plasmodium falciparum malaria: a randomized, double-blind, placebo-controlled trial.

Cerebral malaria: human versus mouse studies.

Caspase-12 dampens the immune response to malaria independently of the inflammasome by targeting NF-kappaB signaling.

Nitric oxide for the adjunctive treatment of severe malaria: hypothesis and rationale.

The Case for the Use of PPARγ Agonists as an Adjunctive Therapy for Cerebral Malaria.

Inhaled nitric oxide reduces endothelial activation and parasite accumulation in the brain, and enhances survival in experimental cerebral malaria.

A phase I clinical study of inhaled nitric oxide in healthy adults.

HIV infection deregulates innate immunity to malaria despite combination antiretroviral therapy.

HIV infection deregulates Tim-3 expression on innate cells: combination antiretroviral therapy results in partial restoration.

Functional roles for C5a and C5aR but not C5L2 in the pathogenesis of human and experimental cerebral malaria.

The importance of motherhood in HIV-positive women of reproductive age in Ontario, Canada.

Murine Plasmodium chabaudi malaria increases mucosal immune activation and the expression of putative HIV susceptibility markers in the gut and genital mucosae.

PPARγ agonists improve survival and neurocognitive outcomes in experimental cerebral malaria and induce neuroprotective pathways in human malaria.

HIV protease inhibitor use during pregnancy is associated with decreased progesterone levels, suggesting a potential mechanism contributing to fetal growth restriction.

Chronic HIV infection impairs nonopsonic phagocytosis of malaria parasites.