IL-5-deficient mice are susceptible to experimental autoimmune encephalomyelitis

Abstract

Experimental autoimmune encephalomyelitis (EAE) is an animal model commonly used to investigate mechanisms involved in the activation of self-reactive T cells. Whereas auto-reactive Th1 cells are believed to be involved in the generation of EAE, Th2 cells can induce EAE in immunocompromised hosts. Since the Th2 cytokine IL-5 can influence the nature and severity of disease, we investigated the role of IL-5 in the EAE model. Wild-type C57BL/6J and IL-5-/- mice were immunized with myelin oligodendrocyte glycoprotein (MOG)35-55 peptide and the development of EAE observed. Our results show that IL-5-/- mice developed EAE with a similar day of onset and comparable severity to wild-type mice. Primed T cells isolated from IL-5-/- mice proliferated equally to wild-type cells in response to antigen challenge with MOG35-55. Antigen-specific T cells from IL-5-/- mice produced IFN-γ and tumor necrosis factor-α, but no IL-4 or IL-10, indicating that a predominant Th1 environment was induced following immunization. No differences in the types of cells infiltrating into the central nervous system were observed between IL-5-/- and wild-type mice. Our results suggest that IL-5 is not directly involved in the initiation or effector phase of MOG35-55-induced EAE in immunocompetent C57BL/6J mice.