Journal
JOURNAL OF NEUROINFLAMMATION
Volume 9, Issue -, Pages -Publisher
BMC
DOI: 10.1186/1742-2094-9-209
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Funding
- Swiss National Science Foundation [310030-132705]
- Swiss Society for Multiple Sclerosis
- Swedish Research Council
- Alfred sterlund's Foundation
- Crafoord Foundation
- Greta and Johan Kock's Foundation
- King Gustaf V's 80th Birthday Foundation
- Hedlund's Foundation
- Swedish Rheumatism Association
- Swedish Society for Medicine
- Torsten Foundation
- Ragnar Sderberg's Foundation
- Royal Physiografic Society
- Ake Wiberg's Foundation
- Hansa Medical AB
- European Committee for Treatment and Research in Multiple Sclerosis (ECTRIMS) Foundation
- Swiss National Science Foundation (Grant) [PP00P3_128372]
- Swiss National Science Foundation (SNF) [PP00P3_128372, 310030_132705] Funding Source: Swiss National Science Foundation (SNF)
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Studies in experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis, have shown that B cells markedly influence the course of the disease, although whether their effects are protective or pathological is a matter of debate. EndoS hydrolysis of the IgG glycan has profound effects on IgG effector functions, such as complement activation and Fc receptor binding, suggesting that the enzyme could be used as an immunomodulatory therapeutic agent against IgG-mediated diseases. We demonstrate here that EndoS has a protective effect in myelin oligodendrocyte glycoprotein peptide amino acid 35-55 (MOG(35-55))-induced EAE, a chronic neuroinflammatory demyelinating disorder of the central nervous system (CNS) in which humoral immune responses are thought to play only a minor role. EndoS treatment in chronic MOG(35-55)-EAE did not impair encephalitogenic T cell priming and recruitment into the CNS of mice, consistent with a primary role of EndoS in controlling IgG effector functions. In contrast, reduced EAE severity coincided with poor serum complement activation and deposition within the spinal cord, suggesting that EndoS treatment impairs B cell effector function. These results identify EndoS as a potential therapeutic agent against antibody-mediated CNS autoimmune disorders.
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