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• W2101465483 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 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." @default.
• W2101465483 created "2016-06-24" @default.
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• W2101465483 creator A5050887342 @default.
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• W2101465483 date "2003-11-01" @default.
• W2101465483 modified "2023-10-07" @default.
• W2101465483 title "IL-5-deficient mice are susceptible to experimental autoimmune encephalomyelitis" @default.
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• W2101465483 doi "https://doi.org/10.1093/intimm/dxg127" @default.
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