T cell function loss in AIDS results in the reaction of Toxoplasma gondii infection and the presentation of this infection as encephalitis (TE). The pathogenesis of this infection is still poorly defined. In order to understand this diseases it is necessary to understand the development of protective immunity to toxoplasmosis in the CNS. Preliminary results indicate that IL4 has an important role in resistance to acute toxoplasmosis in C57BL/6 mice and development of TE in Balb/c mice. These results are suprising since IL4 production is associated with a TH2 which is typically associated with susceptibility to intracellular pathogens such as T. gondii. To gain a better understanding of the role of IL4 in the observed resistance to T. gondii its role in the regulation of IFN_ (the major mediator of resistance to T.gondii) will be examined. In addition the possibility that IL13 can compensate for a loss of IL4 in Balb/c mice will be investigated. The effect of IL4 absence on the development of TE will also be studied and SCID mice used to examine if the observed effects are due to effects of IL4 on T cells or accessory cells. This study has implications for other infectious diseases as well's several atopic and neoplastic disorders. The regulation of the immune system during a response to infection could lead to new therapeutic paradigms and/or approaches to treatment of many diseases as well as prove important in vaccine design.
