| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
Regular Articles |
From the Department of Medical Biochemistry,*
Brain
Inflammation and Immunity Group,
and
Neuropathology Laboratory,
Department of
Pathology, University of Wales College of Medicine, Heath Park,
Cardiff, United Kingdom
This study investigated the capacity of neurons and astrocytes to spontaneously activate the complement system and control activation by expressing complement regulators. Human fetal neurons spontaneously activated complement through the classical pathway in normal and immunoglobulin-deficient serum and C1q binding was noted on neurons but not on astrocytes. A strong staining for C4, C3b, iC3b neoepitope and C9 neoepitope was also found on neurons. More than 40% of human fetal neurons were lysed when exposed to normal human serum in the presence of a CD59-blocking antibody, whereas astrocytes were unaffected. Significant reduction in neuronal cell lysis was observed after the addition of soluble complement receptor 1 at 10 µg/ml. Fetal neurons were stained for CD59 and CD46 and were negative for CD55 and CD35. In contrast, fetal astrocytes were strongly stained for CD59, CD46, CD55, and were negative for CD35. This study demonstrates that human fetal neurons activate spontaneously the classical pathway of complement in an antibody-independent manner to assemble the cytolytic membrane attack complex on their membranes, whereas astrocytes are unaffected. One reason for the susceptibility of neurons to complement-mediated damage in vivo may reside in their poor capacity to control complement activation.
This article has been cited by other articles:
 |
|
 |
|
  J Mocco, W. J. Mack, A. F. Ducruet, S. A. Sosunov, M. E. Sughrue, B. G. Hassid, M. N. Nair, I. Laufer, R. J. Komotar, M. Claire, et al. Complement Component C3 Mediates Inflammatory Injury Following Focal Cerebral Ischemia Circ. Res., July 21, 2006; 99(2): 209 - 217. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 V. S. Ten, S. A. Sosunov, S. P. Mazer, R. I. Stark, C. Caspersen, M. E. Sughrue, M. Botto, E. S. Connolly Jr, and D. J. Pinsky C1q-Deficiency Is Neuroprotective Against Hypoxic-Ischemic Brain Injury in Neonatal Mice Stroke, October 1, 2005; 36(10): 2244 - 2250. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. van Beek, M. van Meurs, B. A. 't Hart, H. P. M. Brok, J. W. Neal, A. Chatagner, C. L. Harris, N. Omidvar, B. P. Morgan, J. D. Laman, et al. Decay-Accelerating Factor (CD55) Is Expressed by Neurons in Response to Chronic but Not Acute Autoimmune Central Nervous System Inflammation Associated with Complement Activation J. Immunol., February 15, 2005; 174(4): 2353 - 2365. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 A. P. KULKARNI, L. A. KELLAWAY, D. K. LAHIRI, and G. J. KOTWAL Neuroprotection from Complement-Mediated Inflammatory Damage Ann. N.Y. Acad. Sci., December 1, 2004; 1035(1): 147 - 164. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 K A Gelderman, H J M A A Zijlmans, M J Vonk, and A Gorter CD55 expression patterns on intestinal neuronal tissue are divergent from the brain Gut, April 1, 2004; 53(4): 507 - 513. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J. VAN BEEK, K. ELWARD, and P. GASQUE Activation of Complement in the Central Nervous System: Roles in Neurodegeneration and Neuroprotection Ann. N.Y. Acad. Sci., May 1, 2003; 992(1): 56 - 71. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. J. Mead, S. K. Singhrao, J. W. Neal, H. Lassmann, and B. P. Morgan The Membrane Attack Complex of Complement Causes Severe Demyelination Associated with Acute Axonal Injury J. Immunol., January 1, 2002; 168(1): 458 - 465. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
