| First Author | Sanchis P | Year | 2020 |
| Journal | Cells | Volume | 9 |
| Issue | 2 | PubMed ID | 32023844 |
| Mgi Jnum | J:302373 | Mgi Id | MGI:6508221 |
| Doi | 10.3390/cells9020330 | Citation | Sanchis P, et al. (2020) Interleukin-6 Derived from the Central Nervous System May Influence the Pathogenesis of Experimental Autoimmune Encephalomyelitis in a Cell-Dependent Manner. Cells 9(2):330 |
| abstractText | BACKGROUND: Interleukin-6 (IL-6) is a pleiotropic and multifunctional cytokine that plays a critical role in induction of experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS). Although EAE has always been considered a peripherally elicited disease, Il6 expression exclusively within central nervous system is sufficient to induce EAE development. Neurons, astrocytes, and microglia can secrete and respond to IL-6. METHODS: To dissect the relevance of each cell source for establishing EAE, we generated and immunized conditional Il6 knockout mice for each of these cell types with myelin oligodendrocyte glycoprotein 35-55 (MOG35-55) peptide dissolved in complete Freund's adjuvant (CFA) and supplemented with Mycobacterium tuberculosis. RESULTS AND CONCLUSIONS: The combined results reveal a minor role for Il6 expression in both astrocytes and microglia for symptomatology and neuropathology of EAE, whereas neuronal Il6 expression was not relevant for the variables analyzed. |
