TREMendous 2 Be Social

Narghes Calcagno; Caroline Baufeld; Charlotte Madore; Oleg Butovsky

doi:10.1016/j.immuni.2018.04.034

TREMendous 2 Be Social

Immunity. 2018 May 15;48(5):842-843. doi: 10.1016/j.immuni.2018.04.034.

Authors

Narghes Calcagno¹, Caroline Baufeld¹, Charlotte Madore¹, Oleg Butovsky²

Affiliations

¹ Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA.
² Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA; Evergrande Center for Immunologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA, USA. Electronic address: obutovsky@rics.bwh.harvard.edu.

Abstract

TREM2 is known for its role in microglial phagocytosis and in neurodegenerative diseases. In this issue of Immunity, Filipello et al. (2018) show that microglial TREM2 is required for synaptic pruning in early development. TREM2-deficient mice show altered social behavior in adulthood, linking TREM2 to neurodevelopmental disease.

Publication types

Comment

MeSH terms

Animals
Brain*
Membrane Glycoproteins
Mice
Microglia*
Neurodegenerative Diseases
Phagocytosis
Receptors, Immunologic
Synapses

Substances

Membrane Glycoproteins
Receptors, Immunologic
Trem2 protein, mouse

Grants and funding

R01 NS088137/NS/NINDS NIH HHS/United States