November 19, 2015
Transcription factor Nr4a1, which regulates the production of norepinephine in macrophages, may be a good target for multiple sclerosis treatment, a mouse model suggests.
Study data, published in Nature Immunology, indicates a previously unknown role for macrophages in neuroinflammation.
“Although multiple sclerosis (MS) is generally considered a T cell-driven disease, many studies have shown that monocytes and monocyte-derived macrophages are also crucial for the development of MS,” Catherine C. Hedrick, PhD, of the Division of Inflammation Biology at La Jolla Institute for Allergy and Immunology in La Jolla, CA told Neurology Advisor. “It is increasingly clear that macrophages recruited in response to inflammation are fundamentally different from homeostatic local microglia within the CNS, and therefore should get special attention for their relevance in initiation and progression of CNS autoimmunity.”
Hedrick and colleagues hypothesized that Nr4a1 may be involved in the interaction of the immune system and sympathetic nervous system in the setting of neuroinflammation. Norepinephrine has previously been shown to play a role in experimental autoimmune encephalitis (EAE), the rodent model of MS. Using an established passive rodent module of EAE to better understand the role of Nr4a1 in CNS autoimmunity, the investigators conducted a series of experiments, including intravital microscopy to observe CNS damage and leukocyte infiltration, flow cytometry to look at the expression of tyrosine hydroxylase (TH), and a mouse macrophage cell line to understand Nr4a1’s regulation of TH.
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