Hofstetter, H. H., A. Y. Karulin, T. G. Forsthuber, P. A. Ott, M. Tary-Lehmann, and P. V. Lehmann. 2005. The cytokine signature of MOG-specific CD4 cells in the EAE of C57BL/6 mice. J. Neuroimmunol. 170:105.

Categories: Autoimmunity

Keywords: Animals / Antigen-Presenting Cells / metabolism / CD4-Positive T-Lymphocytes / immunology / Cytokines / Encephalomyelitis,Autoimmune,Experimental / Epitopes / Glycoproteins / Immunologic Memory / Interferon Type II / biosynthesis / Interleukin-12 / deficiency / Interleukin-2 / Interleukin-4 / blood / Interleukin-6 / Mice / Mice,Inbred C57BL / Mice,Knockout / Myelin-Associated Glycoprotein / Peptide Fragments / Research Support,N.I.H.,Extramural / Research Support,Non-U.S.Gov't / Spleen / cytology

Abstract: Experimental allergic encephalomyelitis (EAE) is an animal model of multiple sclerosis. While EAE is mediated by the cytokines produced by specific T cells, the cytokine signature of these effector cells is unresolved. We tested CD4 cells from MOG peptide 35-55 immunized C57BL/6 mice for their peptide induced cytokine production on antigen presenting cells of the respective cytokine knockout mice, or wild type mice. IL-4 and IL-6 production was seen on wild type antigen presenting cells, suggesting that IL-4 and IL-6 are not T cell products. In contrast, IFN-gamma, IL-2 and IL-3 were found to be produced by the MOG specific CD4 cells. Understanding the cognate vs. bystander cytokine production in EAE might help dissect the contribution of cytokines to the pathogenesis of the disease.