When seen in its entirety, the animal model experimental autoimmune encephalomyelitis (EAE) bears signifi‑cant similarities to multiple sclerosis (MS) and its different varieties. Depending on the model used, EAE may develop in highly distinct forms such as acute, relapsing‑remitting, and primary or even secondary progressive. Although the model was discovered and developed already in the 1930s,[1] it was only in the 1980s that it was clearly proven that T cells are the major driver of disease when mice are immunized by CNS antigen in complete Freund’s adjuvant (CFA). The major evi‑dence came from adoptive transfer experiments using T cell lines in rats and mice.[2‑5] Even though many similarities are observed between MS and its animal model, major concerns still exist about the etiology and the mechanism (s) of disease development of MS. For example, the autoimmune etiology of MS is still questioned and some researches claim that in‑fections with, for example, Epstein–Barr virus, may play an important role in MS immunopathology.[6, 7] Others suggested for some subforms of MS, a primary degenerative scenario with immune‑mediated damage playing a secondary role in the disease.[8‑12] Also, the composition of CNS‑infiltrating cell types differs between EAE and MS; for example, CD8+ T cells, which may be seen as the dominating T cell population in MS histology,[13, 14] are not essential for EAE.[15] Another difference might be the presence and the role of neutrophils in MS versus EAE, with EAE being dependent on neutrophils whereas MS seems to lack a clear association with neutro‑phils. Still, it needs to be emphasized that the pathogenesis in the induced EAE model (but not in spontaneous models) is time wise well controlled and the effect of a certain cellular population can be effectively observed and tested, whereas in MS the timing of the immune response is out of sight and can only be observed during or after acute attacks when the role of populations such as neutrophils may already be blunted.[16] In the standard model most frequently used, EAE is induced by immunization using a water‑in‑oil emulsion of CFA into which the autoantigen such as myelin oligoden‑drocyte glycoprotein (MOG), myelin basic protein (MBP), or proteolipid protein (PLP) is mixed. CFA contains high amounts of heat‑inactivated Mycobacterium tuberculosis. This emulsion is usually injected subcutaneously in the back skin next to the tail base. Also, pertussis toxin injections are given the same day and 2 days later intraperitoneally. EAE normally develops after about 10 days when scores with ascending paralysis usually become visible.