Abstract
The effect of systemic complement depletion by cobra venom factor (CVF) was evaluated in adoptive transfer experimental allergic neuritis (AT-EAN). Spleen cells of rats immunized with a neuritogenic peptide SP26 were injected into naive rats. On days 3 and 6 after cell transfer AT-EAN rats were treated with CVF or saline intraperitoneally. AT-EAN rats treated with CVF had significantly lower scores for histological inflammation (0.25 ± 0.25 vs 1.9 ± 0.4, mean ± SEM, P < 0.03) and demyelination (0.13 ± 0.13 vs 1.6 ± 1.4, P < 0.02) than saline-treated AT-EAN rats. Immunocytochemistry of lumbosacral nerve roots showed significantly less ED1-positive macrophages (0.5 ± 0.3 vs 1.6 ± 0.6, P < 0.04) and CD11bc-positive (expressing complement receptor 3 or CR3) inflammatory cells (0.6 ± 0.4 vs 1.7 ± 0.5, P < 0.03). Our data suggest that complement plays a crucial role in inflammatory demyelination since systemic complement depletion significantly reduces recruitment of macrophages into the nerve and subsequent macrophage-mediated demyelination.
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Received: 24 June 1997 / Revised, accepted: 17 September 1997
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Vriesendorp, F., Flynn, R., Malone, M. et al. Systemic complement depletion reduces inflammation and demyelination in adoptive transfer experimental allergic neuritis. Acta Neuropathol 95, 297–301 (1998). https://doi.org/10.1007/s004010050801
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DOI: https://doi.org/10.1007/s004010050801