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Complement Receptor 2 is increased in cerebrospinal fluid of multiple sclerosis patients and regulates C3 function
Karolinska Inst, Neuroimmunol Unit, Dept Clin Neurosci, S-10401 Stockholm, Sweden.
Karolinska Inst, Neuroimmunol Unit, Dept Clin Neurosci, S-10401 Stockholm, Sweden.
Karolinska Inst, Neuroimmunol Unit, Dept Clin Neurosci, S-10401 Stockholm, Sweden.
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2016 (English)In: Clinical Immunology, ISSN 1521-6616, E-ISSN 1521-7035, Vol. 166, 89-95 p.Article in journal (Refereed) Published
Abstract [en]

Besides its vital role in immunity, the complement system also contributes to the shaping of the synaptic circuitry of the brain. We recently described that soluble Complement Receptor 2 (sCR2) is part of the nerve injury response in rodents. We here study CR2 in context of multiple sclerosis (MS) and explore the molecular effects of CR2 on 0 activation. Significant increases in sCR2 levels were evident in cerebrospinal fluid (CSF) from both patients with relapsing remitting MS (n = 33; 6.2 ng/mL) and secondary-progressive MS (n = 9; 7.0 ng/mL) as compared to controls (n = 18; 4.1 ng/mL). Furthermore, CSF sCR2 levels correlated significantly both with CSF C3 and C1q as well as to a disease severity measure. In vitro, sCR2 inhibited the cleavage and down regulation of Cab to iC3b, suggesting that it exerts a modulatory role in complement activation downstream of C3. These results propose a novel function for CR2/sCR2 in human neuroinflammatory conditions.

Place, publisher, year, edition, pages
2016. Vol. 166, 89-95 p.
Keyword [en]
Complement Receptor 2; Complement system; Multiple sclerosis; Neurodegeneration; Neuroinflammation
National Category
Neurology
Research subject
Medical Science
Identifiers
URN: urn:nbn:se:uu:diva-285294DOI: 10.1016/j.clim.2016.04.003ISI: 000378011500010PubMedID: 27085202OAI: oai:DiVA.org:uu-285294DiVA: diva2:921183
Funder
EU, European Research Council, LSHM-CT-2005-018637Swedish Research CouncilThe Swedish Brain Foundation
Available from: 2016-04-19 Created: 2016-04-19 Last updated: 2017-11-30Bibliographically approved

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Lindblom, RickardNilsson, BoEkdahl Nilsson, Kristina

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