Cytokines in innate and acquired immunity to Trypanosoma cruzi infection.
Resistance to Trypanosoma cruzi infections is critically dependent on cytokine-mediated activation of cell-mediated immune effector mechanisms. This review focuses on the role of IL-10, TNF-alpha, IFN-gamma and IL-12 in controlling T. cruzi replication by the innate and specific immune systems of the vertebrate host. A study performed on mice with disrupted recombinase-activating genes (RAG/KO), which lack T and B lymphocytes, revealed the importance of IL-12, IFN-gamma and TNF-alpha in the resistance against T. cruzi mediated by the innate immune system. In addition, data from experiments using IL-10 KO, RAG/KO and double RAG/IL-10 KO mice indicating an in vivo regulatory role of IL-10 in innate and T. cruzi-specific immunity are discussed.
Abrahamsohn
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IA
Departamento de Imunologia, Universidade de São Paulo, Brasil. iabraham@usp.br
D000818:Animals; D016207:Cytokines / Q000502:physiology*; D007109:Immunity / Q000502:physiology*; D007113:Immunity, Innate / Q000502:physiology*; D007371:Interferon-gamma; D016753:Interleukin-10; D018664:Interleukin-12; D051379:Mice; D018345:Mice, Knockout; D014349:Trypanosoma cruzi / Q000472:pathogenicity*; D014352:Trypanosomiasis / Q000276:immunology*; D014409:Tumor Necrosis Factor-alpha
D016207:Cytokines; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D018664:Interleukin-12; D007371:Interferon-gamma