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Synthetic expansion of brain regulatory T cells effectively prevents neuroinflammatory disease II

ABSTRACT: Synthetic expansion of brain regulatory T cells effectively prevents neuroinflammatory disease II

PROVIDER: PRJNA659543 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12525880_1.fastq.gz	Fastqsanger.gz
	SRR12525880_2.fastq.gz	Fastqsanger.gz
	SRR12525881_1.fastq.gz	Fastqsanger.gz
	SRR12525881_2.fastq.gz	Fastqsanger.gz
	SRR12525882_1.fastq.gz	Fastqsanger.gz

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Synthetic expansion of brain regulatory T cells effectively prevents neuroinflammatory disease II

Project description:An adaptive immunological component to neuroinflammatory diseases is increasingly being recognized. The recent identification and characterization of a small population of regulatory T cells (Tregs) resident in the brain allows for the potential therapeutic exploitation. As the most potent known anti-inflammatory mediators, Tregs have the capacity to reduce inflammation and promote tissue repair, with a key limitation being the small number present in brain tissue. Here we demonstrate that transgenic ‘micro-dosing’ of IL-2 production to the brain allows the efficient expansion of the brain-resident Treg population. This approach, using expression of IL-2 within the normal physiological range but redirected to the brain, allows a 10-fold accumulation of Treg numbers within the brain without any increase in the Treg numbers in circulating or peripheral tissues. No alteration was observed in the frequency or transcriptional profile of non-Treg populations within the brain, and, apart from the numerical expansion, brain-resident Tregs were unaltered in their transcriptional profile. Mice with expanded brain-resident Treg numbers were protected from neuroinflammation and damage in mouse models of traumatic brain injury, stroke and Multiple Sclerosis, with substantial reductions in inflammation and histological damage, and improvements in clinical measurements. To produce a treatment with translational potential, we engineered a viral vector delivery system, capable of specific production of IL-2 in the brain. This treatment approach provided a titratable expansion of brain Tregs, and effective protection against neuroinflammatory disease, with potential translation to the patient context.

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Project description:Manuscript "Molecular markers in the CSF proteome differentiate neuroinflammatory diseases" by Maria L. Elkjaer Arkadiusz Nawrocki, Tim Kacprowski, Anja Hviid Simonsen, Romain Marignier, Tobias Sejbaek, Helle H. Nielsen, Lene Wermuth, Peter Høgh, Finn Sellebjerg, Richard Reynolds, Jan Baumbach, Martin R. Larssen, Zsolt Illes (prepared for submission)

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