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complement in disease aetiology. Genetic variations in complement genes are widespread
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Complement fragments (opsonins; C1q, C3b and iC3b) interact with complement
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complement system is responsible for our defense against pathogens. The complement
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complement system, immune cells, and mediators of inflammation provides an efficient
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complement activation pathway (especially C1q, r, s, and C4) are the strongest
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complement system components (C1QA, C1QB, C1QC, C1S, C1R, C3), microglial
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complement protein C1q or the downstream complement protein C3 exhibit
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complement activation, in producing the necrotizing demyelination seen in the spinal
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complement deposition on synapses followed by microglial engulfment has been
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complement activation can injure tissue. Our study determined whether free
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complement pathway secondary to a not well-understood trigger event
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Complement is increasingly recognized as a context-dependent contributor to cerebral
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complement cascade, a key component of innate immune pathogen defence
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Complement deposition is present in all active white matter lesions
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complement-mediated microglial synaptic engulfment and attenuating synapse loss. These
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complement cascade. The safety and tolerability of ANX005 are currently
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complement cascade (CCC), resulting in leukocyte infiltration of the choroid
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complement components (C) in the adult rat brain and describe
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Complement-mediated synaptic pruning is essential in the developing and healthy
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- Paper Complement activation by ligand-driven juxtaposition of discrete pattern recognition complexes.
complement, the pattern recognition molecules (PRMs) mannan-binding lectin (MBL) and ficolins
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complement inhibitors. Iptacopan, a first-in-class oral factor B inhibitor
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complement components. Gene regulatory network analysis identified TYROBP as the key regulatory
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complement binding, and lipoprotein particle binding. KEGG analysis identified complement
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Complement C5a and C5a receptor levels are increased with PM. C5a is implicated
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complement by intracerebral injection develop characteristic NMO lesions with neuroinflammation
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complement and coagulation cascade. A model based on the 10 most
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complement subnetwork identified by multi-scale gene network studies of postmortem
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complement factors, toll-like receptors, and genetic variants result in Aβ' phagocytosis
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complement factor H (CFH) gene was strongly associated with serum
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complement of these neural systems in comparison to those of other
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