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Single-Cell Transcriptomic and Metabolic Signatures in Exhausted and Classical Memory B Cells-An Exploratory Analysis
Litong Zhu1,2,3,4,5,6, Taoyan Lin7,8, Lai Yee Cheong6
1Division of Nephrology, Nanfang Hospital, Southern Medical University, Guangzhou 510515, China.
Biomedicines
|June 26, 2026
Summary
Disturbances in exhausted and classical memory B cells are linked to systemic lupus erythematosus (SLE) and lupus nephritis (LN). Specific gene expression changes in these B cells correlate with distinct metabolic and immune pathway alterations in SLE and LN patients.
Area of Science:
- Immunology
- Genetics
- Metabolomics
Background:
- Dysregulation of exhausted and classical memory B cells contributes to systemic lupus erythematosus (SLE) and lupus nephritis (LN) pathogenesis.
- The precise genetic mechanisms governing B cell homeostasis in these conditions remain largely unelucidated.
Purpose of the Study:
- To investigate the genetic regulation and molecular pathways associated with exhausted and classical memory B cells in SLE and LN.
- To identify differentially expressed genes (DEGs) and their functional roles in B cell subsets from SLE and LN patients.
Main Methods:
- Analysis of single-cell RNA sequencing data from peripheral blood mononuclear cells (PBMCs) of SLE and LN patients.
- Identification and validation of overlapping DEGs in exhausted and classical memory B cells.
- Gene Ontology (GO) and KEGG pathway analyses to explore associated biological processes and immune signaling, including the JAK-STAT pathway.
- Assessment of relationships between B cell subsets and cellular metabolic pathways.
Main Results:
- Three key DEGs—IFI44L, XAF1, and MX1—were identified in both exhausted and classical memory B cells and validated in B cells from LN patients.
- STAT1 emerged as a central regulator within the protein-protein interaction network of these DEGs.
- Classical memory B cells displayed distinct metabolic profiles, with higher expression of genes involved in sulfur, amino sugar, and butanoate metabolism, contrasting with exhausted B cells.
Conclusions:
- Altered expression of IFI44L, XAF1, and MX1 is significantly associated with unique metabolic signatures and immune pathway dysregulation in exhausted and classical memory B cells.
- These findings provide insights into the genetic and metabolic underpinnings of B cell dysfunction in SLE and LN.
- The study highlights potential therapeutic targets related to specific gene expression and metabolic pathways in B cells for SLE and LN treatment.
