| First Author | Weir C | Year | 2003 |
| Journal | Int Immunol | Volume | 15 |
| Issue | 11 | Pages | 1283-9 |
| PubMed ID | 14565926 | Mgi Jnum | J:110934 |
| Mgi Id | MGI:3652427 | Doi | 10.1093/intimm/dxg127 |
| Citation | Weir C, et al. (2003) IL-5-deficient mice are susceptible to experimental autoimmune encephalomyelitis. Int Immunol 15(11):1283-9 |
| abstractText | 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. |
