Int Immunol. 2003 Nov;15(11):1283-1289
Weir C, Bernard CC, Backstrom BT.
Malaghan Institute of Medical Research, Department of Pathology and Molecular Medicine, Wellington School of Medicine, PO Box 7060, Wellington South, New Zealand Neuroimmunology Laboratory, Department of Biochemistry, La Trobe University, Victoria, 3086, Australia.
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 T(h)1 cells are believed to be involved in the generation of EAE, T(h)2 cells can induce EAE in immunocompromised hosts.
Since the T(h)2 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 MOG(35-55).
Antigen-specific T cells from IL-5(-/-) mice produced IFN-gamma and tumor necrosis factor-alpha, but no IL-4 or IL-10, indicating that a predominant T(h)1 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 MOG(35-55)-induced EAE in immunocompetent C57BL/6J mice.