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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)

Resistance to Encephalitozoon intestinalis is associated with interferon-gamma and interleukin-2 cytokines in infected mice.

The understanding of the immunopathology of infections caused by microsporidia has pinpointed the importance of T cell-mediated immunity. The immunopathology caused by the interesting protozoan parasite Encephalitozoon intestinalis, a microsporidium pathogenic in man, is not clearly understood. In this study, we demonstrate that a specific cellular immune response is implicated in the control of microsporidiosis infection in mice. Interferon (IFN)-gamma receptor knockout mice (IFN-gamma R(o/o)) developed a chronic infection with E. intestinalis, whereas a transient infection developed in wild-type mice. Encephalitozoon intestinalis proteins induced proliferation of murine spleen and mesenteric lymph node cells collected from infected mice. The host response to microsporidia infection was regulated by a specific pattern of cytokine protection. Spleen cells derived from resistant 129 Sv/Ev mice inoculated with E. intestinalis secreted significant levels of gamma-interferon and interleukin-2 but cells from highly susceptible IFN-gamma R knockout mice secreted high levels of interleukin-4 (mostly between 2 and 4 weeks post infection). This is the first report in which a specific cellular immune response against E. intestinalis infection is presented.[1]


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