Remyelination-Promoting Inflammation: Novel Role for MyD88 Signaling in Microglia/Macrophages

Gopal Murugaiyan; Mai Fujiwara; Lucien P Garo

doi:10.1016/j.tins.2020.04.005

Remyelination-Promoting Inflammation: Novel Role for MyD88 Signaling in Microglia/Macrophages

Trends Neurosci. 2020 Jul;43(7):455-457. doi: 10.1016/j.tins.2020.04.005. Epub 2020 Apr 30.

Authors

Gopal Murugaiyan¹, Mai Fujiwara², Lucien P Garo²

Affiliations

¹ Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. Electronic address: mgopal@rics.bwh.harvard.edu.
² Ann Romney Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA.

PMID: 32362400
DOI: 10.1016/j.tins.2020.04.005

Abstract

Inflammation in the central nervous system (CNS) has been linked to demyelination and remyelination. Using zebrafish and mouse models of demyelination and remyelination, Cunha et al. now describe a novel role for myeloid differentiation factor 88 (MyD88) signaling in supporting remyelination by promoting myeloid cell-mediated inflammatory responses via TNF-α, which are essential for phagocytic myelin debris clearance and for oligodendrogenesis.

Keywords: MyD88; TNF-α; demyelination and remyelination; inflammation; microglia and macrophages; multiple sclerosis (MS); oligodendrogenesis.

Publication types

Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't
Comment

MeSH terms

Animals
Demyelinating Diseases*
Inflammation
Macrophages
Mice
Microglia
Myelin Sheath
Myeloid Differentiation Factor 88
Remyelination*

Substances

Myd88 protein, mouse
Myeloid Differentiation Factor 88