Differential Cytokine and Chemokine Production Characterizes Experimental Autoimmune Meningitis and Experimental Autoimmune Encephalomyelitis

• Published in: Clinical immunology (Orlando, Fla.) Fla.), 2000-02, Vol.94 (2), p.114-124
• Main Authors: Perrin, Peter J., Rumbley, Catherine A., Beswick, Richard L., Lavi, Ehud, Phillips, S.Michael
• Format: Article
• Language: English
• Subjects: AIDS/HIV; Amino Acid Sequence; Animals; Autoimmune Diseases - immunology; Autoimmune Diseases - pathology; Biological and medical sciences; Brain - pathology; CD28; CD28 antigen; Chemokines - biosynthesis; Cytokines - biosynthesis; Disease Models, Animal; encephalomyelitis; Encephalomyelitis, Autoimmune, Experimental - immunology; Encephalomyelitis, Autoimmune, Experimental - pathology; Experimental and animal immunopathology. Animal models; IL-2; IL-6; Immunopathology; Lymphocyte Activation; Medical sciences; meningitis; Meningitis - immunology; Meningitis - pathology; Mice; Mice, Inbred C57BL; Molecular Sequence Data; Multiple sclerosis and variants. Guillain barré syndrome and other inflammatory polyneuropathies. Leukoencephalitis; Neurology; Receptors, Chemokine - metabolism; Spleen - cytology; Spleen - immunology; T-Lymphocytes - immunology; Th1 Cells - immunology; Th2 Cells - immunology
• ISSN: 1521-6616; 1521-7035
• DOI: 10.1006/clim.1999.4825

After primary immunization with myelin/oligodendrocyte glycoprotein, CD28−/− mice developed experimental autoimmune meningitis (EAM) rather than experimental autoimmune encephalomyelitis (EAE). Cytokine and chemokine production in EAE and EAM were compared to understand the differences in disease phenotype. T cells from the central nervous system lesions of mice with either EAE or EAM expressed intracellular TNF-α. Splenic T cells from mice with EAM produced TNF-α and IL-6 but no IL-2. Conversely, EAE-derived splenic T cells produced TNF-α and IL-2 but no IL-6. Altered T cell differentiation in EAM was not due to a Th1 to Th2 shift, because equivalent amounts of T cell IFN-γ mRNA were produced in both diseases. Neutrophils also produced inflammatory mediators such as TNF-α and IL-6 in EAM. Autocrine production of MIP-2 mRNA was observed in neutrophils from mice with EAM but not EAE. Therefore, distinct patterns of cytokines and chemokines distinguish EAE and EAM.