Journal
JOURNAL OF NEUROSCIENCE
Volume 31, Issue 11, Pages 3981-3989Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.3617-10.2011
Keywords
-
Categories
Funding
- Japanese Society for Promotion of Sciences
- National Institute on Aging [AG20603, AG27505]
Ask authors/readers for more resources
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-alpha (IFN-alpha), 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-alpha production associated with brain injury or viral infections may inhibit neurogenesis.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available