Complement C3a: Shaping the Plasticity of the Post-stroke Brain

Chapter
Part of the Springer Series in Translational Stroke Research book series (SSTSR)

Abstract

Complement is part of the innate immune system that plays a major role in the initiation of inflammation and host defence against pathogenic bacteria. Complement activation is also a contributor to tissue damage in a range of autoimmune conditions. For those reasons, the activation of the complement system in the central nervous system (CNS) was for long considered deleterious. Based on the evidence accumulated during the past decade, this view has been dramatically changing and complement is gaining recognition for its non-immune surveillance related functions, including regulation of morphogenesis, and adult tissue regeneration. C3a is a 77 amino acid, 9 kDa peptide generated through the proteolytic activation of the central molecule of the complement system, the third complement component, C3. C3a exerts most of its functions through its canonical G-protein coupled receptor C3aR that is expressed by many cell types including neurons and glia. This chapter considers recent insights into the novel roles of the complement system, in particular C3a, in the CNS with focus on brain plasticity and recovery after ischemic brain injury.

Keywords

C3a C3a receptor The complement system Ischemic stroke Neural plasticity Recovery 

Abbreviations

AMPAR

α-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptor

C1q

Complement component 1q

C3

The third complement component

C3a

The smaller of the two fragments generated by proteolytic activation of C3

C3a-desArg

C3a after removal of C-terminal arginine residue

C3aR

C3a receptor

C3b

The larger of the two fragments generated by proteolytic activation of C3

C5a

The smaller of the two fragments generated by proteolytic activation of the fifth complement component

C5aR2

Second receptor for C5a

CD

Cluster of differentiation

CNS

Central nervous system

CR3

Complement receptor 3

ERK

Extracellular signal-regulated kinase

GAP-43

Growth associated protein 43

GFAP

Glial fibrillary acidic protein

GFAP-C3a

Glial fibrillary acidic protein promoter driven expression of C3a

IgG

Immunoglobulin G

IgM

Immunoglobulin M

IL

Interleukin

IXa

Activated coagulation factor IX

MBL

Mannose binding lectin

NGF

Nerve growth factor

XIa

Activated coagulation factor XI

Xa

Activated coagulation factor X

VGLUT1

Vesicular glutamate transporter 1

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Copyright information

© Springer International Publishing AG 2018

Authors and Affiliations

  1. 1.Laboratory of Regenerative Neuroimmunology, Department of Clinical Neuroscience, Institute of Neuroscience and PhysiologySahlgrenska Academy at University of GothenburgGothenburgSweden

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