B Cells at the Cross-Roads of Autoimmune Diseases and Auto-Inflammatory Syndromes

Zouali, Moncef

doi:10.3390/cells11244025

Cited by 6 publications

(5 citation statements)

References 70 publications

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“…germinal center formation and expansion of autoantibody-producing plasma cells typical of lupus pathology [31]. Importantly, blockade of either nicotinic or muscarinic ACh receptors mitigated the effect of ACh on B cells, and systemic delivery of ACh worsened lupus-like manifestations in mice.…”

Section: Adrenergic Modulation Of the Adaptive Immune Responsementioning

confidence: 99%

“…In previous B cell studies, ACh binding to nicotinic receptors was reported to promote plasmablast formation [ 30 ]. More recently, ACh produced locally by spleen FRCs was demonstrated to trigger enhanced lipid oxidation and an autoimmune response characterized by uncontrolled germinal center formation and expansion of autoantibody-producing plasma cells typical of lupus pathology [ 31 ]. Importantly, blockade of either nicotinic or muscarinic ACh receptors mitigated the effect of ACh on B cells, and systemic delivery of ACh worsened lupus-like manifestations in mice.…”

Section: Adrenergic Modulation Of the Adaptive Immune Responsementioning

confidence: 99%

“…B lymphocyte migration and survival also depend on stromal cells, including fibroblastic reticular cells (FRCs). In the spleen, ACh derived from nerve termini or from FRC upregulates expression of CD36 on B cells, which promotes autophagic functions (recycling misfiled and unneeded proteins) and promotes PC differentiation and GC formation [ 30 , 31 ].…”

Section: Figurementioning

confidence: 99%

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Pharmacological and Electroceutical Targeting of the Cholinergic Anti-Inflammatory Pathway in Autoimmune Diseases

Zouali

2023

Pharmaceuticals

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Continuous dialogue between the immune system and the brain plays a key homeostatic role in various immune responses to environmental cues. Several functions are under the control of the vagus nerve-based inflammatory reflex, a physiological mechanism through which nerve signals regulate immune functions. In the cholinergic anti-inflammatory pathway, the vagus nerve, its pivotal neurotransmitter acetylcholine, together with the corresponding receptors play a key role in modulating the immune response of mammals. Through communications of peripheral nerves with immune cells, it modulates proliferation and differentiation activities of various immune cell subsets. As a result, this pathway represents a potential target for treating autoimmune diseases characterized by overt inflammation and a decrease in vagal tone. Consistently, converging observations made in both animal models and clinical trials revealed that targeting the cholinergic anti-inflammatory pathway using pharmacologic approaches can provide beneficial effects. In parallel, bioelectronic medicine has recently emerged as an alternative approach to managing systemic inflammation. In several studies, nerve electrostimulation was reported to be clinically relevant in reducing chronic inflammation in autoimmune diseases, including rheumatoid arthritis and diabetes. In the future, these new approaches could represent a major therapeutic strategy for autoimmune and inflammatory diseases.

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Section: Adrenergic Modulation Of the Adaptive Immune Responsementioning

confidence: 99%

Section: Adrenergic Modulation Of the Adaptive Immune Responsementioning

confidence: 99%

Section: Figurementioning

confidence: 99%

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Pharmacological and Electroceutical Targeting of the Cholinergic Anti-Inflammatory Pathway in Autoimmune Diseases

Zouali

2023

Pharmaceuticals

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“…B-cells are pivotal players in the innate and adaptive immune systems, and any alterations in their functioning can give rise to a range of disorders [ 1 , 2 ]. B-cells are crucial in producing antibodies and mediating the adaptive immune response [ 3 ].…”

Section: Reviewmentioning

confidence: 99%

Guardians of Immunity: Advances in Primary Immunodeficiency Disorders and Management

Peddi,

Vuppalapati,

Sreenivasulu

et al. 2023

Cureus

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Primary immunodeficiency disorders (PIDs) are a heterogeneous group of genetic conditions profoundly impacting immune function. The investigation spans various PID categories, offering insights into their distinct pathogenic mechanisms and clinical manifestations. Within the adaptive immune system, B-cell, T-cell, and combined immunodeficiencies are dissected, emphasizing their critical roles in orchestrating effective immune responses. In the realm of the innate immune system, focus is directed toward phagocytes and complement deficiencies, underscoring the pivotal roles of these components in initial defense against infections. Furthermore, the review delves into disorders of immune dysregulation, encompassing hemophagocytic lymphohistiocytosis (HLH), autoimmune lymphoproliferative syndrome (ALPS), immune dysregulation, polyendocrinopathy, enteropathy, and X-linked(IPEX), and autoimmunity polyendocrinopathy candidiasis-ectodermal dystrophy(APECED), elucidating the intricate interplay between immune tolerance and autoimmunity prevention. Diagnostic strategies for PIDs are explored, highlighting advancements in genetic and molecular techniques that enable precise identification of underlying genetic mutations and alterations in immune function. We have also outlined treatment modalities for PIDs, which often entail a multidisciplinary approach involving immunoglobulin replacement, antimicrobial prophylaxis, and, in select cases, hematopoietic stem cell transplantation. Emerging therapies, including gene therapy, hold promise for targeted interventions. In essence, this review encapsulates the complexity of PIDs, emphasizing the critical importance of early diagnosis and tailored therapeutic interventions. As research advances, a clearer understanding of these disorders emerges, fostering optimism for enhanced patient care and management in the future.

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“…The crucial roles of these B cell subsets have been revealed in different rheumatic diseases such as rheumatoid arthritis [ 7 ], systemic lupus erythematosus [ 8 ], and Sjögren’s syndrome [ 9 ]. B cell subsets also involve in ankylosing spondylitis and other autoinflammatory syndromes [ 10 , 11 ]. A recent study classified AOSD patients into three groups through the peripheral immune cell profiles, showing a significant difference in total B cell frequencies among groups [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

B cell subsets in adult-onset Still’s disease: potential candidates for disease pathogenesis and immunophenotyping

Fang

Xie

et al. 2023

Arthritis Res Ther

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Background Adult-onset Still’s disease (AOSD) is a systemic autoinflammatory disorder of unknown etiology. B cells are critical participants in different rheumatic diseases, and their roles in AOSD are rarely investigated. This study aimed to unveil the B cell subset features in AOSD and provide evidence for B cell-based diagnosis and targeted therapies of AOSD. Methods B cell subsets in the peripheral blood of AOSD patients and healthy controls (HCs) were detected by flow cytometry. Firstly, the frequencies of B cell subsets were compared. Then, the correlation analysis was performed to explore the correlation between B cell subsets and clinical manifestations in AOSD. Finally, unbiased hierarchical clustering was performed to divide AOSD patients into three groups with different B cell subset features, and the clinical characteristics of the three groups were compared. Results The frequencies of B cell subsets were altered in AOSD patients. Disease-promoting subsets (such as naïve B cells, double negative B cells (DN B cells), and plasmablasts) increased, and potential regulatory subsets (such as unswitched memory B cells (UM B cells) and CD24hiCD27+ B cells (B10 cells)) decreased in the peripheral blood of AOSD patients. In addition, the altered B cell subsets in AOSD correlated with the clinical and immunological features, such as immune cells, coagulation features, and liver enzymes. Intriguingly, AOSD patients could be divided into three groups with distinct B cell immunophenotyping: group 1 (naïve B cells-dominant), group 2 (CD27+ memory B cells-dominant), and group 3 (precursors of autoantibody-producing plasma cells-dominant). Moreover, these three group patients demonstrated differential manifestations, including immune cells, liver or myocardial enzymes, coagulation features, and systemic score. Conclusions B cell subsets are significantly altered in AOSD patients, potentially contributing to the disease pathogenesis. These findings would inspire B cell-based diagnosis and targeted therapies for this refractory disease.

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B Cells at the Cross-Roads of Autoimmune Diseases and Auto-Inflammatory Syndromes

Cited by 6 publications

References 70 publications

Pharmacological and Electroceutical Targeting of the Cholinergic Anti-Inflammatory Pathway in Autoimmune Diseases

Pharmacological and Electroceutical Targeting of the Cholinergic Anti-Inflammatory Pathway in Autoimmune Diseases

Guardians of Immunity: Advances in Primary Immunodeficiency Disorders and Management

B cell subsets in adult-onset Still’s disease: potential candidates for disease pathogenesis and immunophenotyping

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