Complement Activation in the Central Nervous System: A Biophysical Model for Immune Dysregulation in the Disease State.

ABSTRACT: Complement, a feature of the innate immune system that targets pathogens for phagocytic clearance and promotes inflammation, is tightly regulated to prevent damage to host tissue. This regulation is paramount in the central nervous system (CNS) since complement proteins degrade neuronal synapses during development, homeostasis, and neurodegeneration. We propose that dysregulated complement, particularly C1 or C3b, may errantly target synapses for immune-mediated clearance, therefore highlighting regulatory failure as a major potential mediator of neurological disease. First, we explore the mechanics of molecular neuroimmune relationships for the regulatory proteins: Complement Receptor 1, C1-Inhibitor, Factor H, and the CUB-sushi multiple domain family. We propose that biophysical and chem

SUBMITTER: Peoples N 

PROVIDER: S-EPMC7969890 | biostudies-literature | 2021

REPOSITORIES: biostudies-literature