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IFN-b acts on monocytes to ameliorate CNS autoimmunity by inhibiting proinflammatory cross-talk between monocytes and Th cells

ABSTRACT: IFN-b acts on monocytes to ameliorate CNS autoimmunity by inhibiting proinflammatory cross-talk between monocytes and Th cells

PROVIDER: PRJNA717301 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14073310_1.fastq.gz	Fastqsanger.gz
	SRR14073310_2.fastq.gz	Fastqsanger.gz
	SRR14073311_1.fastq.gz	Fastqsanger.gz
	SRR14073311_2.fastq.gz	Fastqsanger.gz
	SRR14073312_1.fastq.gz	Fastqsanger.gz

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IFN-b acts on monocytes to ameliorate CNS autoimmunity by inhibiting proinflammatory cross-talk between monocytes and Th cells

Project description:Multiple sclerosis (MS) has been treated with IFN-b for three decades, but the mechanisms underlying its beneficial effects are not well understood. Our study elucidates, in a mouse model of MS, a potential mechanism whereby IFN-b inhibits cooperation between monocytes and T cells, two key immune cell types in MS. We found that IFN-b acts on monocytes to induce secretion of anti-inflammatory molecules, IL-10 and TGF-b, which act on T cells to suppress their production of pro-inflammatory molecules, GM-CSF, TNF, and FASL. Given that these T cell molecules induce proinflammatory features of monocytes, such as IL-1b production, we concluded that IFN-b therapy suppresses cooperation between monocytes and T cells, which otherwise reciprocally amplifies their harmful roles in MS.

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IFN-β Acts on Monocytes to Ameliorate CNS Autoimmunity by Inhibiting Proinflammatory Cross-Talk Between Monocytes and Th Cells.

Project description:IFN-β has been the treatment for multiple sclerosis (MS) for almost three decades, but understanding the mechanisms underlying its beneficial effects remains incomplete. We have shown that MS patients have increased numbers of GM-CSF+ Th cells in circulation, and that IFN-β therapy reduces their numbers. GM-CSF expression by myelin-specific Th cells is essential for the development of experimental autoimmune encephalomyelitis (EAE), an animal model of MS. These findings suggested that IFN-β therapy may function via suppression of GM-CSF production by Th cells. In the current study, we elucidated a feedback loop between monocytes and Th cells that amplifies autoimmune neuroinflammation, and found that IFN-β therapy ameliorates central nervous system (CNS) autoimmunity by inhibiting this proinflammatory loop. IFN-β suppressed GM-CSF production in Th cells indirectly by acting on monocytes, and IFN-β signaling in monocytes was required for EAE suppression. IFN-β increased IL-10 expression by monocytes, and IL-10 was required for the suppressive effects of IFN-β. IFN-β treatment suppressed IL-1β expression by monocytes in the CNS of mice with EAE. GM-CSF from Th cells induced IL-1β production by monocytes, and, in a positive feedback loop, IL-1β augmented GM-CSF production by Th cells. In addition to GM-CSF, TNF and FASL expression by Th cells was also necessary for IL-1β production by monocyte. IFN-β inhibited GM-CSF, TNF, and FASL expression by Th cells to suppress IL-1β secretion by monocytes. Overall, our study describes a positive feedback loop involving several Th cell- and monocyte-derived molecules, and IFN-β actions on monocytes disrupting this proinflammatory loop.

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