International Immunology, Vol. 15, No. 11, pp. 1283-1289,
November 2003
© 2003 Japanese Society for Immunology
IL-5-deficient mice are susceptible to experimental autoimmune encephalomyelitis
1 Malaghan Institute of Medical Research, Department of Pathology and Molecular Medicine, Wellington School of Medicine, PO Box 7060, Wellington South, New Zealand 2 Neuroimmunology Laboratory, Department of Biochemistry, La Trobe University, Victoria, 3086, Australia
Correspondence to: T. Bäckström; E-mail: tbackstrom{at}malaghan.org.nz
Transmitting editor: D. Tarlinton
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-
and tumor necrosis factor-
, 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.
Keywords: autoimmunity, experimental autoimmune encephalomyelitis, IL-5, multiple sclerosis, Th1, Th2
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