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Bhuyan, M. H.

Publications and source records attributed to Bhuyan, M. H..

3 recordsLinked to original sources

An immunophenotype-coupled transcriptomic atlas of mouse hematopoietic progenitors

Decoding the bone marrow (BM) hematopoietic progenitor compartment is central to understanding the development of mature immune cells in health and disease. Single-cell multimodal approaches are transforming the analysis of this heterogeneous compartment by simultaneously capturing transcriptomic and proteomic information. Still, integrated studies covering the full spectrum of murine hematopoietic stem and progenitor cells (HSPCs) remain scarce. Here, we report a Cellular Indexing of Transcriptomes and Epitopes by sequencing (CITE-seq) based atlas of 9,281 low-frequency mouse BM HSPCs, profiled using a 123 antibody-derived tag (ADT) panel coupled with genome-wide single-cell transcriptomes. Multimodal analysis resolved 28 progenitor stages across eight blood lineages, each defined by distinctive surface marker and transcription factor (TF) profiles, and provided novel marker combinations to dissect transcriptionally closely related progenitor stages. Classical mouse progenitor surface markers, such as CD117, CD34, and CD115, were detected in accordance with well-established lineage relationships, whereas CD43 and CD48 showed, unexpectedly, broader expression patterns. Neglected surface molecules such as CD27, CD36, CD106, and PIR-A/B are nominated as novel stage-specific markers. ADT versus transcriptome comparison revealed transcription-translation inconsistencies for markers, including CD54 and CD68. A CITE-seq-guided gating strategy translates these population definitions into FACS-compatible panels for prospective isolation and functional interrogation of previously unresolved progenitor stages. Comprehensive TF network analysis delineated lineage- and stage-specific transcriptional programs. This contributes to clarifying unresolved ontogenies and functions, including the lympho-myeloid dual origin of pDCs or rapid neutrophil turnover. This new and comprehensive resource enables exploration of mouse hematopoietic progenitor states driving discoveries in hematology and immunology.

immunology↗

CITE-seq of murine bone marrow plasmacytoid dendritic cells and haematopoietic progenitor cells in sepsis

This dataset contains single-cell transcriptomic and surface protein profiles of bone marrow cells enriched for plasmacytoid dendritic cells (pDCs) and haematopoietic progenitor populations from septic and sham-operated mice. Sepsis was induced in BALB/c wild-type mice using cecal ligation and puncture (CLP) of moderate severity, with sham surgery as control. Bone marrow was collected 36 hours after surgery, depleted for selected lineage-positive cells by fluorescence-activated cell sorting, and processed using Cellular Indexing of Transcriptomes and Epitopes by Sequencing (CITE-seq). Sample demultiplexing was performed using hashtag oligonucleotides. The dataset includes gene expression matrices, antibody-derived tag counts, and barcode assignments for 13,725 cells, with a comparable distribution of sham and CLP samples across the total cell number. It may be used to study transcriptional states, surface marker expression, and phenotypic diversity of bone marrow cells in sepsis, to compare with other immunological and haematological single-cell datasets, or to train and benchmark computational tools for multimodal single-cell data analysis.

immunology↗

BATF controls IFN I production via DC-SCRIPT in plasmacytoid dendritic cells

The basic leucine zipper ATF-like transcription factor (BATF) plays a pivotal role in coordinating various aspects of lymphoid cell biology, yet essential functions in dendritic cells (DCs) have not been reported. Here we demonstrate that BATF deficiency leads to increased interferon (IFN) I production in Toll-like receptor 9 (TLR9)-activated plasmacytoid dendritic cells (pDCs), while BATF overexpression has an inhibitory effect. BATF-deficient mice exhibit elevated IFN I serum levels early in lymphocytic choriomeningitis virus (LCMV) infection. Through ATAC-Seq analysis, BATF emerges as a pioneer transcription factor, regulating approximately one third of the known transcription factors in pDCs. Integrated transcriptomics and ChIP-Seq approaches identified the transcriptional regulator DC-SCRIPT as a direct target of BATF that suppresses IFN I promoter activity by interacting with the interferon regulatory factor 7 (IRF7). Genome-wide association study (GWAS) analyses further implicate BATF in pDC-mediated human diseases. Our findings establish a novel negative feedback axis in IFN I regulation in pDCs during anti-viral immune responses orchestrated by BATF and DC-SCRIPT, with broader implications for pDC and IFN I-mediated autoimmunity.

immunology↗