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Comparative analysis of B cell receptor repertoires revealed a delay in CD24hiCD38hi transitional B lymphocyte maturation in Multiple Sclerosis patients

ABSTRACT: Comparative analysis of B cell receptor repertoires revealed a delay in CD24hiCD38hi transitional B lymphocyte maturation in Multiple Sclerosis patients

PROVIDER: PRJEB47001 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR6501930_1.fastq.gz	Fastqsanger.gz
	ERR6501930_2.fastq.gz	Fastqsanger.gz
	ERR6501940_1.fastq.gz	Fastqsanger.gz
	ERR6501940_2.fastq.gz	Fastqsanger.gz
	ERR6501950_1.fastq.gz	Fastqsanger.gz

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Comparative analysis of B cell receptor repertoires revealed a delay in CD24hiCD38hi transitional B lymphocyte maturation in Multiple Sclerosis patients

Project description:To analyse properties of clonal BCR sequences of transitional and total B cells from peripheral blood of patients with highly active and benign MS compared to healthy donors

2021-08-23 | E-MTAB-10859 | biostudies-arrayexpress

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Project description:Klhl6 belongs to the KLHL gene family, which is composed of an N-terminal BTB-POZ domain and 4 to 6 Kelch motifs in tandem. Several of these proteins function as adaptors of the Cullin3 E3 ubiquitin ligase complex. Here we report that Klhl6 deficiency induces, as previously described, a two-fold reduction in mature B cells. However, we find that this deficit is centered on the inability of transitional T1 B cells to survive and to progress toward the T2 B cell stage, whereas cells that have passed this step generate normal germinal centers upon a T-dependent immune challenge. Klhl6-deficient T1 B cells showed a two-fold over-expression of genes linked with cell proliferation, including most targets of the APC/C complex, a set of genes whose expression is precisely down-modulated upon culture of splenic transitional B cells in presence of BAFF. These results thus suggest a delay in the differentiation process of Klhl6-deficient B cells between the immature and transitional stage. We further show, in the BL2 Burkitt’s lymphoma cell line, that KLHL6 interacts with Cullin3, but also that it binds to HBXIP/Lamtor5, a protein involved in cell cycle regulation and cytokinesis. Finally, we report that KLHL6, which is recurrently mutated in B cell lymphomas, is an off-target of the normal somatic hypermutation process taking place in germinal center B cells in both mice and humans, thus leaving open, whether, in spite of the lack of impact of Klhl6 deficiency on germinal center B cell expansion, mutants could contribute to the oncogenic process.

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