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Murine complement C4 is not required for experimental autoimmune encephalomyelitis by Laura A. Boos; Alexander J. Szalai; Scott R. Barnum is a Neuroscience article available to read on EtoBox.

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## Abstract In vitro studies have demonstrated that myelin and myelin‐derived proteins activate both the classical and alternative complement pathways. More recently, studies have shown that mice deficient in factor B, a protein required for activation of the alternative pathway, have attenuated experimental autoimmune encephalomyelitis (EAE), the animal model for multiple sclerosis. The relative contribution of the classical pathway to the pathogenesis of EAE has remained unexplored. To address this question, we performed EAE using mice deficient in C4 (C4^−/−^), a protein required for full activation of the classical pathway. We found that deletion of the __C4__ gene does not significantly change either the time of onset or the severity and tempo of myelin oligodendrocyte‐induced EAE compared with controls with a fully intact complement system. We observed similar levels of cellular infiltration (CD11b^+^ macrophages and CD3^+^ T cells) and demyelination in the two kinds of mice. Despite this, ribonuclease protection assays demonstrated a two‐ to fourfold increase in several pro‐inflammatory cytokines in C4^−/−^ mice with EAE, including interleukin‐β (IL‐1β), IL‐18, tumor necrosi

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Author

Laura A. Boos; Alexander J. Szalai; Scott R. Barnum

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley; Research Square (ISSN 0894-1491)

Published

2004

Language

EN

Field

Neuroscience (Life Sciences)