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Loss of the molecular clock in myeloid cells exacerbates T cell-mediated CNS autoimmune disease.

Abstract：

:The transcription factor BMAL1 is a core component of the molecular clock, regulating biological pathways that drive 24 h (circadian) rhythms in behaviour and physiology. The molecular clock has a profound influence on innate immune function, and circadian disruption is linked with increased incidence of multiple sclerosis (MS). However, the mechanisms underlying this association are unknown. Here we show that BMAL1 and time-of-day regulate the accumulation and activation of various immune cells in a CNS autoimmune disease model, experimental autoimmune encephalomyelitis (EAE). In myeloid cells, BMAL1 maintains anti-inflammatory responses and reduces T cell polarization. Loss of myeloid BMAL1 or midday immunizations to induce EAE create an inflammatory environment in the CNS through expansion and infiltration of IL-1β-secreting CD11b+Ly6Chi monocytes, resulting in increased pathogenic IL-17+/IFN-γ+ T cells. These findings demonstrate the importance of the molecular clock in modulating innate and adaptive immune crosstalk under autoimmune conditions.

journal_name

Nat Commun

journal_title

Nature communications

authors

Sutton CE,Finlay CM,Raverdeau M,Early JO,DeCourcey J,Zaslona Z,O'Neill LAJ,Mills KHG,Curtis AM

doi

10.1038/s41467-017-02111-0

subject

Has Abstract

pub_date

2017-12-12 00:00:00

pages

1923

issue

1

issn

2041-1723

pii

10.1038/s41467-017-02111-0

journal_volume

8

pub_type

杂志文章

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