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Impaired TIGIT expression on B cells drives circulating follicular helper T cell expansion in multiple sclerosis

ABSTRACT: Impaired TIGIT expression on B cells drives circulating follicular helper T cell expansion in multiple sclerosis

PROVIDER: PRJNA869957 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR21082940_1.fastq.gz	Fastqsanger.gz
	SRR21082940_2.fastq.gz	Fastqsanger.gz
	SRR21082941_1.fastq.gz	Fastqsanger.gz
	SRR21082941_2.fastq.gz	Fastqsanger.gz
	SRR21082942_1.fastq.gz	Fastqsanger.gz

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Impaired TIGIT expression on B cells drives circulating follicular helper T cell expansion in multiple sclerosis

Project description:B cell depletion in patients with relapsing remitting multiple sclerosis (RRMS) markedly prevents new MRI lesions and disease activity, suggesting the hypothesis that altered B cell function leads to the activation of T cells driving disease pathogenesis. Here, we performed comprehensive analyses of memory B cells from patients with MS and healthy age-matched controls stimulated with CD40L and IL-21, modeling the help of follicular helper T cells (Tfh cells), and found a differential gene expression signature in multiple B cell pathways. Most striking was impaired TIGIT expression on MS-derived B cells mediated by dysregulation of the transcription factor TCF4. Activated circulating Tfh cells (cTfh cells) expressed CD155, the ligand of TIGIT, and TIGIT on B cells revealed their capacity to suppress the proliferation of IL-17-producing cTfh cells via TIGIT/CD155 axis. Finally, CCR6+ cTfh cells were significantly increased in MS and their frequency was inversely correlated with that of TIGIT+ B cells. Together, these data suggest that the dysregulation of negative feedback loops between TIGIT+ memory B cells and cTfh cells in MS drive the activated immune system in the disease.

2022-10-19 | GSE211358 | GEO

Impaired TIGIT expression on B cells drives circulating follicular helper T cell expansion in multiple sclerosis.

Project description:B cell depletion in patients with relapsing-remitting multiple sclerosis (RRMS) markedly prevents new MRI-detected lesions and disease activity, suggesting the hypothesis that altered B cell function leads to the activation of T cells driving disease pathogenesis. Here, we performed comprehensive analyses of CD40 ligand- (CD40L-) and IL-21-stimulated memory B cells from patients with MS and healthy age-matched controls, modeling the help of follicular helper T cells (Tfh cells), and found a differential gene expression signature in multiple B cell pathways. Most striking was the impaired TIGIT expression on MS-derived B cells mediated by dysregulation of the transcription factor TCF4. Activated circulating Tfh cells (cTfh cells) expressed CD155, the ligand of TIGIT, and TIGIT on B cells revealed their capacity to suppress the proliferation of IL-17-producing cTfh cells via the TIGIT/CD155 axis. Finally, CCR6+ cTfh cells were significantly increased in patients with MS, and their frequency was inversely correlated with that of TIGIT+ B cells. Together, these data suggest that the dysregulation of negative feedback loops between TIGIT+ memory B cells and cTfh cells in MS drives the activated immune system in this disease.

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Transcription profiling of mouse vivo follicular helper CD4 T cells (TFH) versus non follicular helper CD4 T cells (non-TFH)

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