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Transcriptome analysis of TACI-deficient and WT naïve T cells

ABSTRACT: Transcriptome analysis of TACI-deficient and WT naïve T cells

PROVIDER: PRJNA638270 | ENA |

REPOSITORIES: ENA

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Transcriptome analysis of TACI-deficient and WT naïve T cells

Project description:TACI (transmembrane activator and calcium modulator and cyclophilin ligand interactor) plays critical roles in B cells by promoting immunoglobulin class-switching and plasma cell survival. However, its expression and function in T cells remain controversial. In this study, we found that TACI deficiency in mice results in expansion of TH17 and Treg populations. To understand the mechanisms underlying increased frequencies and numbers of TH17 cells correlated with more severe colitis in TACI-/- mice, microarray-based transcriptome analysis was conducted to identify genes that were differentially expressed in TACI-/- vs WT naive CD4+ T cells.

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scRNASeq of Naïve, GC, plasma, memory B cells sorted from WT and Fip200-deficient mice spleen

Project description:We have employed a scRANSeq to study the difference between WT and Fip200-deficient B cell populations from mice spleen 11 days after immunization. FIP200 plays an important role in regulating LC3-dependent and LC3-independent autophage pathway, which is crucial for B cell development and differentiation. This study presents the transcriptome of Naive, GC, plasma and memory B cell populations at the peak of mice immune-response and provides new insights into the role of FIP200 in regulating plasma differentiation. FIP200f/fMb1Cre+/- (KO) mice and their littermatecontrol, FIP200f/fMb1Cre-/-(WT) were immunized with 50 ug NP29-KLH with Alum, then splenocytes isolated from WT and KO mice 11 days after immunization were enriched for GC, plasma, and memory B cells by depleting non-B cells and IgDhi B cells using magnetic beads. Those enriched samples were then barcoded and sorted for naïve, GC, plasma, and memory B cells, which were then mixed for single-cell RNA sequencing.

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Multi-omics Analysis of naive B cells of patients harboring the C104R mutation in TACI

Project description:Common variable immunodeficiency (CVID) is the most prevalent form of symptomatic primary immunodeficiency in humans. The genetic cause of CVID is still unknown in about 70% of cases. 10% of CVID patients carry heterozygous mutations in the tumor necrosis factor receptor superfamily member 13B gene (TNFRSF13B), encoding TACI. Mutations in TNFRSF13B alone may not be sufficient for the development of CVID, as 1% of the healthy population carry these mutations. The common hypothesis is that TACI mutations are not fully penetrant and additional factors contribute to the development of CVID. To determine these additional factors, we investigated the perturbations of transcription factor (TF) binding and the transcriptome profiles in unstimulated and CD40L/IL21-stimulated naïve B cells from CVID patients harboring the C104R mutation in TNFRSF13B and compared them to their healthy relatives with the same mutation. In addition, the proteome of stimulated naïve B cells was investigated. For functional validation, intracellular protein concentrations were measured by flow cytometry. Our analysis revealed 8% less accessible chromatin in unstimulated naïve B cells and 25 % less accessible chromatin in class-switched memory B cells from affected and unaffected TACI mutation carriers compared to healthy donors. The most enriched TF binding motifs in TACI mutation carriers involved members from the ETS, IRF and NF-B TF families. Validation experiments supported dysregulation of the NF-B and MAPK pathways. In steady state, naïve B cells had increased cell death pathways and reduced cell metabolism pathways; while after stimulation, enhanced immune responses and decreased cell survival was detected. Using a multi-omics approach, our findings provide valuable insights into the impaired biology of naïve B cells from TACI mutation carriers.

2022-10-14 | PXD035459 | Pride

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