Abstract
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.
Highlights
The central nervous system (CNS) has been traditionally described as an immune-privileged environment
Regarding complement modulation in the setting of CNS neoplastic disease, major frontiers in complement-targeted therapeutics in glioma are likely to include a focus on C1qtargeted therapeutics, given its consistent role in driving tumor progression, as well as C3-targeted therapeutics in the context of radiation to limit radiation-induced edema and degeneration allowing for maximal treatment dosing
As presented in this review, complement modulation has been implicated in the development and progression of brain and spine tumors as well as cell injury in the peritumoral environment
Summary
The central nervous system (CNS) has been traditionally described as an immune-privileged environment. In both in-vitro and in-vivo models, glioblastoma was shown to upregulate the expression of the C1-INH protein that prevents the assembly of the C1 complex and inhibits the initiation of complement activation via the classical pathway [50]. Expression of CD55 and CD59 could theoretically inhibit complement activation at the surface of growing GBM tumors in vivo, and CD59 overexpression has been observed in human glioma samples [60].
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