Complement receptor 2 is expressed in neural progenitor cells and regulates adult hippocampal neurogenesis.

Citation data:

The Journal of neuroscience : the official journal of the Society for Neuroscience, ISSN: 1529-2401, Vol: 31, Issue: 11, Page: 3981-9

Publication Year:
2011
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Repository URL:
https://digitalcommons.wustl.edu/open_access_pubs/220
PMID:
21411641
DOI:
10.1523/jneurosci.3617-10.2011
PMCID:
PMC3071463
Author(s):
Moriyama, Maiko; Fukuhara, Takeshi; Britschgi, Markus; He, Yingbo; Narasimhan, Ramya; Villeda, Saul; Mollina, Hector; Huber, Brigitte T; Holers, Mike; Wyss-Coray, Tony
Publisher(s):
Society for Neuroscience
Tags:
Neuroscience
article description
Injury and inflammation are potent regulators of adult neurogenesis. As the complement system forms a key immune pathway that may also exert critical functions in neural development and neurodegeneration, we asked whether complement receptors regulate neurogenesis. We discovered that complement receptor 2 (CR2), classically known as a coreceptor of the B-lymphocyte antigen receptor, is expressed in adult neural progenitor cells (NPCs) of the dentate gyrus. Two of its ligands, C3d and interferon-α (IFN-α), inhibited proliferation of wild-type NPCs but not NPCs derived from mice lacking Cr2 (Cr2(-/-)), indicating functional Cr2 expression. Young and old Cr2(-/-) mice exhibited prominent increases in basal neurogenesis compared with wild-type littermates, whereas intracerebral injection of C3d resulted in fewer proliferating neuroblasts in wild-type than in Cr2(-/-) mice. We conclude that Cr2 regulates hippocampal neurogenesis and propose that increased C3d and IFN-α production associated with brain injury or viral infections may inhibit neurogenesis.