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Sex-specific differences in the function and differentiation of ABCs contribute to the female bias in lupus pathogenesis

ABSTRACT: Sex-specific differences in the function and differentiation of ABCs contribute to the female bias in lupus pathogenesis

PROVIDER: PRJNA732180 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR14627700_1.fastq.gz	Fastqsanger.gz
	SRR14627700_2.fastq.gz	Fastqsanger.gz
	SRR14627701_1.fastq.gz	Fastqsanger.gz
	SRR14627701_2.fastq.gz	Fastqsanger.gz
	SRR14627702_1.fastq.gz	Fastqsanger.gz

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Sex-specific differences in the function and differentiation of ABCs contribute to the female bias in lupus pathogenesis

Project description:We report the application of RNA-seq, ATAC-seq, and CUT and RUN technology for high-throughput profiling of H3K27me3 epigenetic marks in mice SWAP-70 and DEF6 double knockout (DKO) B-lymphocytes (ABCs and FoBs) flow sorted from spleen. We show that ABCs from female and male DKO mice have unique transcriptional profiles, chromatin accessibility, and that there is a selective loss of repressive chromatin marks like H3K27me3 in ABCs of DKO females can contribute to the increased expression of X-chromosome linked genes like Tlr7 and several other loci among which Tbx21, the classical ABC marker, showed strongest loss in F-ABCs as compared to F-FoBs.

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IL-13Ra1-mediated signaling regulates ABC expansion and lupus pathogenesis

Project description:ABCs are an emerging B cell subset that aberrantly expand in SLE. ABC generation and differentiation exhibit marked sexual dimorphism and TLR7 engagement is a key contributor to these sex differences. ABC generation is also controlled by IL-21 and its interplay with IFNg and IL-4. Here we investigated whether IL-13Ra1, an X-linked receptor that transmits IL-4/IL-13 signals, can regulate ABCs and lupus pathogenesis.

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RNA-seq data of ABC from Bm12-induced lupus model

Project description:Age-associated B cells (ABCs) accumulate in systemic autoimmunity, and contributes to pathogenesis. ABCs are characterized by high expression of CD11c and T-bet. As a transcription factor, T-bet cannot be labeled in live cells with antibodies, so we constructed a reporter mouse strain in which fluorescent protein tdTomato fused to T-bet. Then we sorted ABCs (CD11c+T-bet+CD21- B cell) and non-ABCs (CD11c-T- bet- B cell) from the Bm12-induced lupus model for RNA sequencing.

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Project description:To characterize age-associated B cells (ABCs), we performed single-cell RNA and BCR sequencing on splenic B-lineage cells from a murine lupus model induced by Toll-like receptor 7 (TLR7) stimulation and on peripheral blood B-lineage cells from a treatment-naïve patient with systemic lupus erythematosus (SLE). We identified a population of ABCs with features of plasmablast precursors (pre-PB ABCs). In the TLR7-induced lupus model, B cell-specific Commd3 deletion reduced the frequency of pre-PB ABCs and was associated with increased apoptosis in this population.

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Project description:Systemic lupus erythematosus (SLE) is the prototypic systemic autoimmune disease. It is thought that many common variant gene loci of weak effect act additively to predispose to common autoimmune diseases, while the contribution of rare variants remains unclear. Here we describe that rare coding variants in lupus-risk genes are present in most SLE patients and healthy controls. We demonstrate the functional consequences of rare and low frequency missense variants in the interacting proteins BLK and BANK, which are present alone, or in combination, in a substantial proportion of lupus patients. The rare variant found in patients, but not those found exclusively in controls, impair suppression of IRF and type-I IFN in human B cell lines and increase pathogenic lymphocytes in lupus-prone mice. Thus, rare gene variants are common in SLE and likely contribute to genetic risk.

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Functional rare and low frequency variants in BLK and BANK contribute to human lupus pathogenesis

Project description:Functional rare and low frequency variants in BLK and BANK contribute to human lupus pathogenesis

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B cell-intrinsic IFN-g promotes CD11c+ age-associated B cell differentiation and compromises affinity-based germinal center selection in lupus

Project description:Lupus patients respond less efficiently to vaccinations and are more susceptible to infections. Previously, we have shown, in lupus models, that excessive CD11c+ age-associated B cells (ABCs) not only contribute to autoantibody production but also compromise antigen-specific germinal center (GC) B cell selection and affinity maturation by promoting aberrant T cell activation. Yet, how CD11c+ ABC differentiation is regulated is not fully understood. Here we show that B cell-intrinsic IFN-γ is required for excessive CD11c+ ABC differentiation in lupus mice. B cell-intrinsic IFN-γ is mainly produced by CD11c+ ABCs. IFN-γ-deficiency leads to decreased expression of ABC characteristic genes, including Zeb2, an ABC-specific transcription factor recently described. We further show that ablating IFN-γ can normalize T cell overactivation and rescue antigen-specific GC responses in lupus mice. Our study offers insight into the crucial role of B cell-intrinsic IFN-γ in promoting CD11c+ ABC differentiation and compromising affinity-based germinal center selection and affinity maturation in lupus, providing a potential target for lupus treatment.

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Project description:The molecular basis for the female bias of systemic lupus erythematosus remains unclear. We sought to determine the fidelity of dynamic X-chromosome inactivation maintenance in the pathogenesis of murine models of spontaneous lupus, including the heavily female-biased NZM2328 model.

2022-09-20 | GSE213318 | GEO

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Project description:Specific metabolic program is required for generation of immune cells and their proper function. Since the description of age-associated or autoimmune-associated B cells (ABCs), there has been a growing interest in the role of these cells in autoimmunity. ABCs have many distinct functional properties, including antigen presentation to T cells and autoantibody production in lupus mouse models. Metabolic properties which support these functions are unknown in ABCs. In this study, we showed that ABCs are metabolically hyperactivated than follicular (FO) B cells. There was an increased glycolysis and oxidative phosphorylation (OXPHOS) in ABCs. In line with this observation, ABCs express key costimulatory molecules for T cell activation with distinct group of cytokines. T cell proliferation and activation were induced by both FO B and ABCs in antigen-dependent manner. However, ABCs induce stronger T cell receptor signaling from naïve CD4+ T cells, leading to differentiation of follicular helper T (Tfh) cells. ABCs actively internalize OVA protein and increased autophagy formation. Treatment of ABCs with metformin suppressed antigen presentation by decreasing antigen uptake, leading to a defective generation of Tfh cells. Taken together, these findings reveal distinct metabolic activity in ABCs and define fundamental connection between metabolism and function within ABCs.

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IL-13Ra1-mediated signaling regulates ABC expansion and lupus pathogenesis

Project description:IL-13Ra1-mediated signaling regulates ABC expansion and lupus pathogenesis

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