Pivotal role of interleukin-12 and interferon-γ axis in controlling tissue parasitism and inflammation in the heart and central nervous system during Trypanosoma cruzi infection
Michailowsky V, Silva NM, Rocha CD et al. Pivotal role of interleukin-12 and interferon-γ axis in controlling tissue parasitism and inflammation in the heart and central nervous system during Trypanosoma cruzi infection. Am J Pathol 2001; 159: 1723-1733.
Defective nitric oxide effector functions lead to extreme susceptibility of Trypanosoma cruzi-infected mice deficient in gamma interferon receptor or inducible nitric oxide synthase
Holscher C, Kolher G, Muller U et al. Defective nitric oxide effector functions lead to extreme susceptibility of Trypanosoma cruzi-infected mice deficient in gamma interferon receptor or inducible nitric oxide synthase. Infect Immun 1998; 66: 1208-1215.
Activation of Toll-like receptor-2 by glycosylphosphatidylinositol anchors from a parasitic protozoan
Campos MAS, Almeida IC, Takeuchi O et al. Activation of Toll-like receptor-2 by glycosylphosphatidylinositol anchors from a parasitic protozoan. J Immunol 2001; 167: 416-423.
Impaired production of proinflammatory cytokines and host resistance to acute infection with Trypanosoma cruzi in mice lacking functional myeloid differentiation factor 88
Campos XM, Closel M, Valente EP et al. Impaired production of proinflammatory cytokines and host resistance to acute infection with Trypanosoma cruzi in mice lacking functional myeloid differentiation factor 88. J Immunol 2004; 172: 1711-1718.
Highly purified glycosylphosphatidylinositols from Trypanosonza cruzi are potent proinflammatory agents
Almeida IC, Camargo MM, Procopio DO et al. Highly purified glycosylphosphatidylinositols from Trypanosonza cruzi are potent proinflammatory agents. EMBO J 2000; 19: 1476-1485.
Requirement of mitogen-activated protein kinases and I kappa B phosphorylation for induction of proinflammatory cytokines synthesis by macrophages indicates functional similarity of receptors triggered by glycosylphosphatidylinositol anchors from parasitic protozoa and bacterial lipopolysaccharide
Ropert C, Almeida IC, Closel M et al. Requirement of mitogen-activated protein kinases and I kappa B phosphorylation for induction of proinflammatory cytokines synthesis by macrophages indicates functional similarity of receptors triggered by glycosylphosphatidylinositol anchors from parasitic protozoa and bacterial lipopolysaccharide. J Immunol 2001; 166: 3423-3431.
Glycoinositolphospholipids from Trypanosoma cruzi interfere with macrophages and dendritic cell responses
Brodskyn C, Patricio J, Oliveira R et al. Glycoinositolphospholipids from Trypanosoma cruzi interfere with macrophages and dendritic cell responses. Infect Immun 2000; 70 3736-3743.
The Trypanosoma cruzi trans-sialidase, through its COOH-terminal tandem repeat, upregulates interleukin 6 secretion in normal human intestinal microvascular endothelial cells and peripheral blood mononuclear cells
Saavedra E, Herrera M, Gao W et al. The Trypanosoma cruzi trans-sialidase, through its COOH-terminal tandem repeat, upregulates interleukin 6 secretion in normal human intestinal microvascular endothelial cells and peripheral blood mononuclear cells. J Exp Med 1999; 190: 1825-1836.
DNA from protozoan parasites Babesia bovis, Trypanosoma cruzi, and T. brucei is mitogenic for B lymphocytes and stimulates macrophage expression of interleukin-12, tumor necrosis factor alpha, and nitric oxide
Shoda LK, Kegerreis KA, Suarez CE et al. DNA from protozoan parasites Babesia bovis, Trypanosoma cruzi, and T. brucei is mitogenic for B lymphocytes and stimulates macrophage expression of interleukin-12, tumor necrosis factor alpha, and nitric oxide. Infect Immun 2001; 69: 2162-2171.
Inhibition of a p38/stress-activated protein kinase-2-dependent phosphatase restores function of IL-1 receptor-associate kinase-1 and reverses Toll-like receptor 2- and 4-dependent tolerance of macrophages
Ropert C, Closel M, Chaves AC et al. Inhibition of a p38/stress-activated protein kinase-2-dependent phosphatase restores function of IL-1 receptor-associate kinase-1 and reverses Toll-like receptor 2- and 4-dependent tolerance of macrophages. J Immunol 2003; 171: 1456-1465.