Inflammation plays a key role in the pathophysiology of Glioblastoma Multiforme (GBM). Here we focus on the contribution of the so far largely ignored complement system.ELISA and immunohistochemistry were combined to assess levels and localization of critical components of the initiation- and effector pathways of the complement cascade in sera and tumor tissue from GBM patients and matched controls.Serum levels of factor-B were decreased in GBM patients whereas C1q levels were increased. C1q and factor-B deposited in the tumor tissue. Deposition of C3 and C5b-9 suggests local complement activation. MBL deficiency, based on serum levels, was significantly less frequent among GBM patients compared to controls (14% vs. 33%). Therefore low levels of MBL may protect against the initiation/progression of GBM.

C1q, Complement system, Factor B, Glial tumor, Glioblastoma multiforme, Mannose binding lectin (MBL)
dx.doi.org/10.1016/j.jneuroim.2014.11.016, hdl.handle.net/1765/87264
Journal of Neuroimmunology
Department of Neurosurgery

Bouwens van der Vlis, T.A.M, Trouw, L.A, Veerhuis, R, Dirven, C.M.F, Lamfers, M.L.M, & Al-Khawaja, H. (2015). Complement activation in Glioblastoma Multiforme pathophysiology: Evidence from serum levels and presence of complement activation products in tumor tissue. Journal of Neuroimmunology, 278, 271–276. doi:10.1016/j.jneuroim.2014.11.016