it is possible that this decrease in SLAMF1 and SLAMF6 expression could also play a role in the iNKT positive selection defect, similar to what we demonstrated recently in c-Myb knockout mice. However cMyb-defective thymocytes had also a defect in the expression of SAP, the signaling molecule required downstream SLAMs, and we did not observe any alterations in SAP expression in dnRas thymocytes. Further experiments will be required to assess the possible contribution of the SLAMF1 and SLAMF6 expression defect to the iNKT cell selection phenotype. In conclusion, in this manuscript we present genetic evidence supporting a critical role of Ras, and its downstream effectors Egr1 and Egr-2 for positive selection of iNKT cells, suggesting that the signaling pathways emanating from the TCR during positive selection of conventional ab T cells and iNKT cells are similar. It will be important to characterize how this signaling component cooperates with signals derived from the SLAM/SAP axis to initiate the molecular program that characterizes this lineage, including expression of PLZF. JEV, a flavivirus causes acute encephalopathy in children. High mortality, representing over 20% has been reported. The clinical manifestations of infection include fever, headache, vomiting, signs of meningeal irritation, and altered consciousness. JEV infection thus, targets the CNS leading to high mortality. In survivors, the morbidity is high due to lingering neurological and/or psychiatric deficits in a large proportion of patients. Current therapeutic interventions for JE are symptomatic and no cure is available. The principle cells, which respond to JEV infection are the microglia in the CNS. Microglia are known to be involved in the immune surveillance of the brain. They are the immune effector cells and undergo extensive morphological changes from resting to activated state following JEV challenge. Morphological changes are accompanied by extensive proliferation and chemotaxis resulting in release of mediators that trigger massive inflammatory response. Thus, JEV infection in CNS is characterized by extensive recruitment of microglia followed by release of proinflammatory molecules that are the prime mediators of neuropathological changes associated with JE. Inflammatory response in JE acts as a double-edged sword where it protects from initial damage and is involved in repair process leading to neuroprotection. However, extensive microglial activation acts as a driving force resulting in irreversible damage. The activated microglia release excessive amounts of cytokines, chemokines, eicosanoids including leukotrienes, particularly leukotriene B4 and prostaglandins. A complex interplay exists between eicosanoids including leukotrienes, prostaglandins produced from arachidonic acid on one hand and cytokines/ chemokines on the other. Thus, limiting the extensive microgliosis accompanying JE could potentially halt the progression of events leading to mortality and morbidity caused by JEV infection. Peroxisome proliferator-activated receptor-a is one of the members of nuclear receptor PPAR family and is a modulator of inflammation. Fenofibrate is an agonist of PPARa and leads to its activation promoting the expression of neuroprotective genes, which trigger both anti-oxidant and anti-inflammatory response.