Effects of stress on thymic B cells in C57BL/6J mice: phenotypic characterization and mechanistic insights
- 1Postdoctoral Research Station in Basic Medicine, Hebei Medical University
- 2Collaborative Innovation Center of Forensic Medical Molecular Identification, Hebei Key Laboratory of Forensic Medicine, Department of Forensic Medicine, Hebei Medical University
Abstract
Introduction: As an important cause of immune system dysfunction, stress can damage thymic stromal cells, leading to a persistent imbalance in thymic function. Thymic B cells can present autoantigens, playing a critical role in the establishment of central T cell tolerance. However, current research on the effects of stress on thymic B cells remains limited.
Methods: Publicly available scRNA-seq datasets were analyzed to characterize thymic B cell phenotypes and glucocorticoid responsiveness. A restraint stress mouse model was employed to assess stress-induced changes in thymic B cell abundance and phenotype by flow cytometry and histopathology, and transcriptomic alterations by bulk RNA sequencing of sorted thymic B cells.
Results: Thymic B cells exhibited a distinctive memory B cell signature with constitutively activated immune-related pathways, and robust glucocorticoid responsiveness. Restraint stress significantly reduced thymic B cell numbers, increased the proportion of IgD ⁺ IgM ⁺ B cells, and downregulated the expression of CD80 and CD86 in IgD ⁺ IgM ⁺ B cells. Transcriptomic profiling revealed that stress suppressed cell cycle and G2/M checkpoint pathway, inhibited CD40L- and IFN-λ-responsive gene expression, attenuated Aire-dependent gene expression, and diminished the presentation of autoantigens. Furthermore, the expression levels of CD40 and MHC II in most of the thymic B cell subsets were markedly decreased.
Discussion: This study reveals the detrimental impact of stress on thymic B cell. Collectively, stress impairs thymic B cell proliferation and attenuates critical licensing signals, including the CD40L–CD40 and IFN-λ signaling, thereby leading to a reduction in thymic B cell numbers, compromised activation, and impaired antigen-presenting capacity.
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BibTeX
@article{ma2026effects,
title = {{Effects of stress on thymic B cells in C57BL/6J mice: phenotypic characterization and mechanistic insights}},
author = {Longda Ma and Weibo Shi and Songjun Wang and Bin Cong},
journal = {Frontiers in Immunology},
year = {2026},
month = oct,
doi = {10.3389/fimmu.2026.1963346},
url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1963346/full},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Effects of stress on thymic B cells in C57BL/6J mice: phenotypic characterization and mechanistic insights
AU - Longda Ma
AU - Weibo Shi
AU - Songjun Wang
AU - Bin Cong
PY - 2026
DA - 2026/10/13
JO - Frontiers in Immunology
DO - 10.3389/fimmu.2026.1963346
UR - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1963346/full
AB - Introduction: As an important cause of immune system dysfunction, stress can damage thymic stromal cells, leading to a persistent imbalance in thymic function. Thymic B cells can present autoantigens, playing a critical role in the establishment of central T cell tolerance. However, current research on the effects of stress on thymic B cells remains limited. Methods: Publicly available scRNA-seq datasets were analyzed to characterize thymic B cell phenotypes and glucocorticoid responsiveness. A restraint stress mouse model was employed to assess stress-induced changes in thymic B cell abundance and phenotype by flow cytometry and histopathology, and transcriptomic alterations by bulk RNA sequencing of sorted thymic B cells. Results: Thymic B cells exhibited a distinctive memory B cell signature with constitutively activated immune-related pathways, and robust glucocorticoid responsiveness. Restraint stress significantly reduced thymic B cell numbers, increased the proportion of IgD ⁺ IgM ⁺ B cells, and downregulated the expression of CD80 and CD86 in IgD ⁺ IgM ⁺ B cells. Transcriptomic profiling revealed that stress suppressed cell cycle and G2/M checkpoint pathway, inhibited CD40L- and IFN-λ-responsive gene expression, attenuated Aire-dependent gene expression, and diminished the presentation of autoantigens. Furthermore, the expression levels of CD40 and MHC II in most of the thymic B cell subsets were markedly decreased. Discussion: This study reveals the detrimental impact of stress on thymic B cell. Collectively, stress impairs thymic B cell proliferation and attenuates critical licensing signals, including the CD40L–CD40 and IFN-λ signaling, thereby leading to a reduction in thymic B cell numbers, compromised activation, and impaired antigen-presenting capacity.
SN - 1664-3224
ER -