| Summary |
Multiple Sclerosis is an autoimmune disease involving the degradation of myelin by one's own immune cells. Modifying the behavior of the population of cells responsible for causing the disease could lead to alleviation of symptoms and increased quality of life. Experimental autoimmune encephalomyelitis (EAE), the animal model used herein, is similar to MS in respect to destruction of nervous tissue. Various cytokines (IL-IRA, IL-2, IL-4, IL-13, IL-16, and IFN[beta]) were expressed as recombinant proteins with an attached neuroantigen (a portion of myelin basic protein) in an effort to modify the activity of cells responsible for destruction of myelin. These cytokine/antigen fusion proteins were assayed for activity of both the cytokine and the neuroantigen regions. In all cases, the fusion proteins were shown to modify the behavior of T-cells and/or macrophages. Additionally, cytokine/antigen fusion proteins were shown to preferentially load antigen into the class II MHC pathway. Whole MBP protein with or without free cytokine did not elicit as strong of a response as cytokine/antigen fusion protein. These data suggest that cytokine fused with neuroantigen can be used to target specific cell populations and modify cell behavior in ways that free cytokine and neuroantigen cannot. |
