Aberrant expression of inhibitory receptors on B cells in patients with Graves’ disease

Liu, Yalei; Feng, Yu; Tang, Shu; Zhang, Lijun; Huang, Zhenfeng; Shi, Xiasheng; Fang, Yuanyuan; Yang, Junpeng; Deng, Xinru; Wang, Limin; Liu, Xiaozhuan; Yuan, Huijuan

doi:10.1016/j.humimm.2021.12.001

Cited by 3 publications

(5 citation statements)

References 39 publications

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“…4A ) [ 63 ]. MZB have also been reported to have low levels of CD23 and high expression of the inhibitory receptor CD32b [ 138 , 139 ]. Recently, two distinct populations of MZB have been described that differ in cell surface properties, transcriptional factors, and distribution in lymphoid tissues [ 6 ].…”

Section: Naïve B Cellsmentioning

confidence: 99%

Human B-cell subset identification and changes in inflammatory diseases

Velounias

Tull

2022

Clinical and Experimental Immunology

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Our understanding of the B cell subsets found in human blood and their functional significance has advanced significantly in the past decade. This has been aided by the evolution of high dimensional phenotypic tools such as mass cytometry and single cell RNA sequencing which have revealed heterogeneity in populations that were previously considered homogenous. Despite this, there is still uncertainty and variation between studies as to how B cell subsets are identified and named. This review will focus on the most commonly encountered subsets of B cells in human blood and will describe gating strategies for their identification by flow and mass cytometry. Important changes to population frequencies and function in common inflammatory and autoimmune diseases will also be described.

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Section: Naïve B Cellsmentioning

confidence: 99%

Human B-cell subset identification and changes in inflammatory diseases

Velounias

Tull

2022

Clinical and Experimental Immunology

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“…The frequency of circulating PCs (CD19+CD27 high CD38 high ) was analyzed by flow cytometry and found to be higher in GD patients than controls [ 55 ]. Overall, the percentage of lymphocytes that are B cells are reportedly higher in GD patients than in healthy controls, although the previously cited study by Cao found no difference [ 61 , 66 ]. Similarly, the absolute counts of B cells appear to be higher in GD patients than controls [ 35 ].…”

Section: B Cellsmentioning

confidence: 91%

“…Researchers have examined the proportions of B cells subsets in GD patients. GD patients appear to have fewer IgM memory B cells (IgM+IgD+CD27+), pre-switched memory B cells (CD27+IgD+), and conventional memory B cells (CD27+IgD−) than healthy controls [ 32 , 61 ]. Conversely, GD patients have more double-negative B cells (IgD−CD27−) and naïve B cells (CD27−IgD+) [ 32 , 61 ].…”

Section: B Cellsmentioning

confidence: 99%

“…GD patients appear to have fewer IgM memory B cells (IgM+IgD+CD27+), pre-switched memory B cells (CD27+IgD+), and conventional memory B cells (CD27+IgD−) than healthy controls [ 32 , 61 ]. Conversely, GD patients have more double-negative B cells (IgD−CD27−) and naïve B cells (CD27−IgD+) [ 32 , 61 ]. The proportions of double-negative B cells were also found to be positively correlated with both TRAb and TSAb [ 32 ].…”

Section: B Cellsmentioning

confidence: 99%

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Characterizing the Interplay of Lymphocytes in Graves’ Disease

Hansen

Johnson

Weber

et al. 2023

IJMS

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Graves’ disease (GD) is a thyroid-specific autoimmune disease with a high prevalence worldwide. The disease is primarily mediated by B cells, which produce autoantibodies against the thyroid-stimulating hormone receptor (TSHR), chronically stimulating it and leading to high levels of thyroid hormones in the body. Interest in characterizing the immune response in GD has motivated many phenotyping studies. The immunophenotype of the cells involved and the interplay between them and their secreted factors are crucial to understanding disease progression and future treatment options. T cell populations are markedly distinct, including increased levels of Th17 and follicular helper T cells (Tfh), while Treg cells appear to be impaired. Some B cells subsets are autoreactive, and anti-TSHR antibodies are the key disease-causing outcome of this interplay. Though some consensus across phenotyping studies will be discussed here, there are also complexities that are yet to be resolved. A better understanding of the immunophenotype of Graves’ disease can lead to improved treatment strategies and novel drug targets.

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“…This cascade amplifies autoantibody production, inflicting substantial harm to the host. Our previous study has proved abnormal distribution of B-cell subsets occur in the presence of GD ( Liu Y. et al., 2022 ), yet the exact mechanisms initiating this immune response remain to be fully understood.…”

Section: Introductionmentioning

confidence: 99%

Alteration in gut microbiota is associated with immune imbalance in Graves’ disease

Liu,

Tang,

Feng

et al. 2024

Front. Cell. Infect. Microbiol.

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BackgroundGraves’ disease (GD), characterized by immune aberration, is associated with gut dysbiosis. Despite the growing interest, substantial evidence detailing the precise impact of gut microbiota on GD’s autoimmune processes remains exceedingly rare.ObjectiveThis study was designed to investigate the influence of gut microbiota on immune dysregulation in GD.MethodsIt encompassed 52 GD patients and 45 healthy controls (HCs), employing flow cytometry and enzyme-linked immunosorbent assay to examine lymphocyte and cytokine profiles, alongside lipopolysaccharide (LPS) levels. Gut microbiota profiles and metabolic features were assessed using 16S rRNA gene sequencing and targeted metabolomics.ResultsOur observations revealed a disturbed B-cell distribution and elevated LPS and pro-inflammatory cytokines in GD patients compared to HCs. Significant differences in gut microbiota composition and a marked deficit in short-chain fatty acid (SCFA)-producing bacteria, including ASV263(Bacteroides), ASV1451(Dialister), and ASV503(Coprococcus), were observed in GD patients. These specific bacteria and SCFAs showed correlations with thyroid autoantibodies, B-cell subsets, and cytokine levels. In vitro studies further showed that LPS notably caused B-cell subsets imbalance, reducing conventional memory B cells while increasing naïve B cells. Additionally, acetate combined with propionate and butyrate showcased immunoregulatory functions, diminishing cytokine production in LPS-stimulated cells.ConclusionOverall, our results highlight the role of gut dysbiosis in contributing to immune dysregulation in GD by affecting lymphocyte status and cytokine production.

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Aberrant expression of inhibitory receptors on B cells in patients with Graves’ disease

Cited by 3 publications

References 39 publications

Human B-cell subset identification and changes in inflammatory diseases

Human B-cell subset identification and changes in inflammatory diseases

Characterizing the Interplay of Lymphocytes in Graves’ Disease

Alteration in gut microbiota is associated with immune imbalance in Graves’ disease

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