Multiple sclerosis (MS) is a common neurologic and autoimmune disorder. The development of this disease is under the control of both genetic and environmental factors. Environmental elements such as sun exposure, viral exposition or smoking contribute to MS occurrence. This thesis is based on a compilation of a selection of my publications. We first assessed signaling molecular pathways of CD4+ T cells and could identify elements, which in addition to their link with environment, shape the immune response during experimental autoimmune encephalomyelitis (EAE), an animal model of MS. For examples the aryl hydrocarbon receptor (AhR) controls cytokines secretion and is identified as the receptor of dioxin, a toxin that is potentially lethal; metallothioneins (MTs) negatively regulate Interleukin-10 production but are suited as sensors for heavy metals. I further oriented my research toward immunometabolism and studied the role of the lipid metabolites and T cell migration to the CNS during EAE.