Caroline Junqueira

The endless race between Trypanosoma cruzi and host immunity: lessons for and beyond Chagas disease.

Trypanosoma cruzi as an effective cancer antigen delivery vector.

Trypanosoma cruzi adjuvants potentiate T cell-mediated immunity induced by a NY-ESO-1 based antitumor vaccine.

Identification and functional analysis of Trypanosoma cruzi genes that encode proteins of the glycosylphosphatidylinositol biosynthetic pathway.

Blockade of CTLA-4 promotes the development of effector CD8+ T lymphocytes and the therapeutic effect of vaccination with an attenuated protozoan expressing NY-ESO-1.

Induction of Inhibitory Receptors on T Cells During Plasmodium vivax Malaria Impairs Cytokine Production.

Virus-like Particle Display of the α-Gal Carbohydrate for Vaccination against Infection.

Down Modulation of Host Immune Response by Amino Acid Repeats Present in a Ribosomal Antigen.

Comparative transcriptome profiling of virulent and non-virulent Trypanosoma cruzi underlines the role of surface proteins during infection.

New Vaccine Formulations Containing a Modified Version of the Amastigote 2 Antigen and the Non-Virulent CL-14 Strain Are Highly Antigenic and Protective against Challenge.

Cytotoxic CD8 T cells recognize and kill Plasmodium vivax-infected reticulocytes.

The immunology of Plasmodium vivax malaria.

Decidual NK Cells Transfer Granulysin to Selectively Kill Bacteria in Trophoblasts.

Contributions of IFN-γ and granulysin to the clearance of Plasmodium yoelii blood stage.

Caspase-8 mediates inflammation and disease in rodent malaria.

Author Correction: Caspase-8 mediates inflammation and disease in rodent malaria.

γδ T cells suppress Plasmodium falciparum blood-stage infection by direct killing and phagocytosis.

Improved Performance of ELISA and Immunochromatographic Tests Using a New Chimeric A2-Based Protein for Human Visceral Leishmaniasis Diagnosis.

SARS-CoV-2 infects blood monocytes to activate NLRP3 and AIM2 inflammasomes, pyroptosis and cytokine release.

FcγR-mediated SARS-CoV-2 infection of monocytes activates inflammation.

Inflammasome activation in infected macrophages drives COVID-19 pathology.