Acta Neuropathologica

, Volume 134, Issue 2, pp 325–327 | Cite as

NG2 plays a role in neuroinflammation but is not expressed by immune cells

  • Maja Kitic
  • Khalad Karram
  • Nicole Israel
  • Nir Yogev
  • Sonja M. Lacher
  • Yilang Tang
  • Hatice Yigit
  • Jan Bauer
  • Florian Wanke
  • Anela Knezovic
  • Jacqueline Trotter
  • Florian C. Kurschus
  • Ari Waisman

Nerve/glial antigen 2 (NG2) is a large transmembrane chondroitin sulphate proteoglycan expressed mainly by oligodendrocyte precursor cells in the developing and adult central nervous system (CNS) and pericytes in various organs throughout the body [14]. Numerous studies reported increased levels of this molecule after CNS injury, but its relevance remained questionable [5, 6, 9, 11].

In recent years, contradicting studies have been published concerning the role of NG2 molecule in experimental autoimmune encephalomyelitis (EAE). Using an immunization protocol consisting of two 100 μg doses of MOG35–55, emulsified in CFA, on days 0 and 7 and two injections of 300 ng of pertussis toxin on days 0 and 2 post-immunization, Moransard et al. demonstrated that NG2 is dispensable for EAE development [11]. In contrast, Ferrara et al. reported recently that mice of the same NG2-deficient line displayed milder EAE clinical score [4]. Of note, the latter group used a different immunization protocol...



We thank Michaela Blanfeld, Elena Zurkowski and Alexei Nikolaev for excellent technical support. This work was financed by the Deutsche Forschunsgemeinschaft (DFG) Grant CRC TRR128 to AW, FCK and JT and by European Union, FP7-PEOPLE-2012-ITN NeuroKine to AW.

Compliance with ethical standards

All experiments were performed in accordance with relevant guidelines and regulations of the central animal facility of the Johannes Gutenberg University Mainz.

Conflict of interest

The authors declare that they have no conflict of interest.

Supplementary material

401_2017_1735_MOESM1_ESM.pdf (178 kb)
Supplementary material 1 (PDF 178 kb)
401_2017_1735_MOESM2_ESM.docx (134 kb)
Supplementary material 2 (DOCX 134 kb)


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Copyright information

© Springer-Verlag Berlin Heidelberg 2017

Authors and Affiliations

  1. 1.Institute for Molecular MedicineUniversity Medical Center of the Johannes Gutenberg University MainzMainzGermany
  2. 2.Department of Biology, Molecular Cell BiologyJohannes Gutenberg University MainzMainzGermany
  3. 3.Department of Neuroimmunology, Center for Brain ResearchMedical University of ViennaViennaAustria

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