scholarly journals Modulation of the Complement System by Neoplastic Disease of the Central Nervous System

2021 ◽  
Vol 12 ◽  
Author(s):  
Steven K. Yarmoska ◽  
Ali M. Alawieh ◽  
Stephen Tomlinson ◽  
Kimberly B. Hoang

The complement system is a highly conserved component of innate immunity that is involved in recognizing and responding to pathogens. The system serves as a bridge between innate and adaptive immunity, and modulation of the complement system can affect the entire host immune response to a foreign insult. Neoplastic diseases have been shown to engage the complement system in order to evade the immune system, gain a selective growth advantage, and co-opt the surrounding environment for tumor proliferation. Historically, the central nervous system has been considered to be an immune-privileged environment, but it is now clear that there are active roles for both innate and adaptive immunity within the central nervous system. Much of the research on the role of immunological modulation of neoplastic disease within the central nervous system has focused on adaptive immunity, even though innate immunity still plays a critical role in the natural history of central nervous system neoplasms. Here, we review the modulation of the complement system by a variety of neoplastic diseases of the central nervous system. We also discuss gaps in the current body of knowledge and comment on future directions for investigation.

2009 ◽  
Vol 12 (2) ◽  
pp. 179-192 ◽  
Author(s):  
Trent M. Woodruff ◽  
Rahasson R. Ager ◽  
Andrea J. Tenner ◽  
Peter G. Noakes ◽  
Stephen M. Taylor

Cells ◽  
2021 ◽  
Vol 10 (7) ◽  
pp. 1812
Author(s):  
Marcela Pekna ◽  
Milos Pekny

The complement system, an effector arm of the innate immune system that plays a critical role in tissue inflammation, the elimination of pathogens and the clearance of dead cells and cell debris, has emerged as a regulator of many processes in the central nervous system, including neural cell genesis and migration, control of synapse number and function, and modulation of glial cell responses. Complement dysfunction has also been put forward as a major contributor to neurological disease. Astrocytes are neuroectoderm-derived glial cells that maintain water and ionic homeostasis, and control cerebral blood flow and multiple aspects of neuronal functioning. By virtue of their expression of soluble as well as membrane-bound complement proteins and receptors, astrocytes are able to both send and receive complement-related signals. Here we review the current understanding of the multiple functions of the complement system in the central nervous system as they pertain to the modulation of astrocyte activity, and how astrocytes use the complement system to affect their environment in the healthy brain and in the context of neurological disease.


2019 ◽  
Vol 10 ◽  
Author(s):  
Robb Wesselingh ◽  
Helmut Butzkueven ◽  
Katherine Buzzard ◽  
David Tarlinton ◽  
Terence J. O'Brien ◽  
...  

2016 ◽  
Vol 138 (5) ◽  
pp. 653-693 ◽  
Author(s):  
Katrin I. Andreasson ◽  
Adam D. Bachstetter ◽  
Marco Colonna ◽  
Florent Ginhoux ◽  
Clive Holmes ◽  
...  

2014 ◽  
Vol 9 (6) ◽  
pp. 565-571 ◽  
Author(s):  
Kelly A. Meulendyke ◽  
Joshua D. Croteau ◽  
M. Christine Zink

2019 ◽  
Vol 19 (1S) ◽  
pp. 68-70
Author(s):  
N A Didkovsky ◽  
I K Malashenkova ◽  
D P Ogurtsov ◽  
S A Krynskiy ◽  
N A Hailov ◽  
...  

The aim of the work is to study the level of systemic inflammation and changes in adaptive immunity in the early period after acute psychosis to assess their participation in the pathogenesis of alcoholic mental and cognitive disorders. We examined 28 patients with alcoholic psychosis (AP) and a control group of 17 healthy volunteers. Indicators of systemic inflammation and immunity, including key cytokines and lymphocyte subpopulations, were investigated. After acute psychosis of patients with alcoholism, pronounced activation of humoral immunity with impaired clearance of immune complexes, increased content and activity of Th2 with signs of insufficiency and dysfunction of Th1, reduced content and activity of cytotoxicity system cells and signs of systemic inflammation (increased CRP, cortisol, cytokines). Activation of Th2 response and an excess of proinflammatory mediators in patients with AP through various ways of interaction with the Central nervous system (n. vagus, choroidal plexus of the ventricles, and others) can participate in the disorders of metabolism of neurotransmitters in the Central nervous system involved in the pathogenesis of alcoholism, and in the maintenance of neuroinflammation. A high level of systemic inflammation can be both a trigger of psychosis and a manifestation of violations of neuroimmune interactions, as well as the development of excitotoxicity and damage to neurons in acute psychosis.


2008 ◽  
Vol 198 (7) ◽  
pp. 1028-1036 ◽  
Author(s):  
Matthias Klein ◽  
Bianca Obermaier ◽  
Barbara Angele ◽  
Hans‐Walter Pfister ◽  
Hermann Wagner ◽  
...  

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