Protein kinase C-theta is required for development of experimental cerebral malaria.
Fauconnier, Mathilde; Bourigault, Marie-Laure; Meme, Sandra; Szeremeta, Frederic; Palomo, Jennifer; Danneels, Adeline; Charron, Sabine; Fick, Lizette; Jacobs, Muazzam; Beloeil, Jean-Claude; Ryffel, Bernhard; Quesniaux, Valerie F J.
Am J Pathol
; 178(1): 212-21, 2011 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-21224058
Perivascular Arrest of CD8+ T Cells Is a Signature of Experimental Cerebral Malaria.
IFN-Î³-producing CD4+ T cells promote experimental cerebral malaria by modulating CD8+ T cell accumulation within the brain.
Phosphatidylinositol 3-Kinase Î³ is required for the development of experimental cerebral malaria.
Immunobiology of Plasmodium in liver and brain.
Suppression of CD4+ Effector Responses by Naturally Occurring CD4+ CD25+ Foxp3+ Regulatory T Cells Contributes to Experimental Cerebral Malaria.
Gamma Interferon Mediates Experimental Cerebral Malaria by Signaling within Both the Hematopoietic and Nonhematopoietic Compartments.
Critical role of IL-33 receptor ST2 in experimental cerebral malaria development.
Cannabinoid Receptor 2 Modulates Susceptibility to Experimental Cerebral Malaria through a CCL17-dependent Mechanism.
The C-type lectin receptor DCIR is crucial for the development of experimental cerebral malaria.
Protein kinase C Î¸ deficiency increases resistance of C57BL/6J mice to Plasmodium berghei infection-induced cerebral malaria.