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Cells
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B Lymphocytes in Auto-Inflammatory Diseases
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B Lymphocytes in Auto-Inflammatory Diseases

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Immunology".

Deadline for manuscript submissions: closed (30 April 2023) | Viewed by 17112

Special Issue Editor

Dr. Moncef M. Zouali

E-Mail Website
Guest Editor
1. Graduate Institute of Biomedical Sciences, China Medical University Taichung, Taichung, Taiwan
2. Institute National de la Santé et de la Recherche Médicale (INSERM), Paris, France
Interests: immune tolerance; autoimmunity; epigenetics; B lymphocytes; innate immunity; biotherapeutics
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Ever since their discovery, B lymphocytes have gained wide attraction because of their importance in immune defense against a large number of threats. B cells play a pivotal role in the adaptive branch of the immune system by producing high-affinity antibodies, secreting anti-inflammatory cytokines, and presenting antigens to T cells. The existence of different B cell subsets (regulatory B cells, marginal zone B cells, follicular B cells) exhibiting distinct functional properties further provides the immune system with additional mechanisms to cope with potential threats. In parallel, B lymphocytes take part in the innate arm of the immune system by expressing Toll-like receptors, producing pro-inflammatory cytokines cytokines and potentially protective natural antibodies that pre-exist to exposure to pathogens. Studies of the phenotype of mice lacking B cells revealed that this cell subset is involved in 1) lymphoid organogenesis through expression of lymphotoxin-a1b2, 2) generation of follicular dendritic networks, 3) formation of follicle-associated epithelium in Peyer’s patches, 4) differentiation of CD+ T cells and of a non-canonical subset of NK T cells, and 4) even tissue repair in the liver. In human, B cell depletion reduces inflammatory Th17 cells. Additionally, the cross-talk of B cells with various other cell types, such as neutrophils and cells of the skeletal and the neuro-endocrine systems, and the fact that they express components of the inflammasome that acts as a modulator of the innate and adaptive immune systems, further account for the multiple roles of B cells in auto-inflammatory diseases. Given the multifaceted functions of B cells in mammals, they are involved in the pathogenesis of several inflammatory disorders, and B cell targeting represents a promising therapeutic strategy for a wide range of disorders, from neurological to cardiovascular diseases. A more profound understanding of the biology and functions of B cell subsets and their interplay with a variety of other cell types will be important for designing novel immuno-intervention strategies for a variety of auto-inflammatory diseases.

Dr. Moncef M. Zouali
Guest Editor

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Keywords

  • B lymphocyte
  • autoimmunity
  • immune tolerance
  • autoimmune disease
  • cross-talk
  • treatment
  • adaptive immunity
  • innate immunity

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Published Papers (5 papers)

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Research

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15 pages, 2506 KiB  
Article
A Study on MDA5 Signaling in Splenic B Cells from an Imiquimod-Induced Lupus Mouse Model with Proteomics
by Yu-Jih Su, Fu-An Li, Jim Jinn-Chyuan Sheu, Sung-Chou Li, Shao-Wen Weng, Feng-Chih Shen, Yen-Hsiang Chang, Huan-Yuan Chen, Chia-Wei Liou, Tsu-Kung Lin, Jiin-Haur Chuang and Pei-Wen Wang
Cells 2022, 11(21), 3350; https://doi.org/10.3390/cells11213350 - 24 Oct 2022
Cited by 3 | Viewed by 2973
Abstract
Introduction: Several environmental stimuli may influence lupus, particularly viral infections. In this study, we used an imiquimod-induced lupus mouse model focused on the TLR7 pathway and proteomics analysis to determine the specific pathway related to viral infection and the related protein expressions in [...] Read more.
Introduction: Several environmental stimuli may influence lupus, particularly viral infections. In this study, we used an imiquimod-induced lupus mouse model focused on the TLR7 pathway and proteomics analysis to determine the specific pathway related to viral infection and the related protein expressions in splenic B cells to obtain insight into B-cell responses to viral infection in the lupus model. Materials and Methods: We treated FVB/N wild-type mice with imiquimod for 8 weeks to induce lupus symptoms and signs, retrieved splenocytes, selected B cells, and conducted the proteomic analysis. The B cells were co-cultured with CD40L+ feeder cells for another week before performing Western blot analysis. Panther pathway analysis was used to disclose the pathways activated and the protein–protein interactome was analyzed by the STRING database in this lupus murine model. Results: The lupus model was well established and well demonstrated with serology evidence and pathology proof of lupus-mimicking organ damage. Proteomics data of splenic B cells revealed that the most important activated pathways (fold enrichment > 100) demonstrated positive regulation of the MDA5 signaling pathway, negative regulation of IP-10 production, negative regulation of chemokine (C-X-C motif) ligand 2 production, and positive regulation of the RIG-I signaling pathway. A unique protein–protein interactome containing 10 genes was discovered, within which ISG15, IFIH1, IFIT1, DDX60, and DHX58 were demonstrated to be downstream effectors of MDA5 signaling. Finally, we found B-cell intracellular cytosolic proteins via Western blot experiment and continued to observe MDA5-related pathway activation. Conclusion: In this experiment, we confirmed that the B cells in the lupus murine model focusing on the TLR7 pathway were activated through the MDA5 signaling pathway, an important RNA sensor implicated in the detection of viral infections and autoimmunity. The MDA5 agonist/antagonist RNAs and the detailed molecular interactions within B cells are worthy of further investigation for lupus therapy. Full article
(This article belongs to the Special Issue B Lymphocytes in Auto-Inflammatory Diseases)
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14 pages, 2562 KiB  
Article
B Cells Specific CpG Induces High IL-10 and IL-6 Expression In Vitro in Neuro-Behçet’s Disease
by Olfa Maghrebi, Meriam Belghith, Cyrine Jeridi, Amine Rachdi, Fatma Nabli Fatnassi, Zakaria Saied, Samir Belal, Samia Ben Sassi and Mohamed-Ridha Barbouche
Cells 2022, 11(8), 1306; https://doi.org/10.3390/cells11081306 - 12 Apr 2022
Cited by 7 | Viewed by 2548
Abstract
Remitting-RelapsingMultiple Sclerosis (RRMS) and Neuro-Behçet Disease (NBD) are two chronic neuroinflammatory disorders leading to neurological damage. Herein, we investigated in these patients the IL-10-producing cells during the early stages of these disorders. Cellular and molecular investigations were carried out on treatment naive patients [...] Read more.
Remitting-RelapsingMultiple Sclerosis (RRMS) and Neuro-Behçet Disease (NBD) are two chronic neuroinflammatory disorders leading to neurological damage. Herein, we investigated in these patients the IL-10-producing cells during the early stages of these disorders. Cellular and molecular investigations were carried out on treatment naive patients suffering from RRMS and NBD recruited at the first episode of clinical relapse. Our findings demonstrate that CSF-B cells from NBD patients, but not RRMS, are the major source of intrathecal IL-10 as compared to T-CD4 cells. Moreover, we showed a lower expression of TGF-β and IL35, in the CSF cells of NBD patients as compared to the control group. Specific in vitro CpG stimulation of peripheral blood B cells from NBD patients resulted in a concomitant early mRNA expression of IL6 and IL10 but was limited to IL10 for RRMS patients. Furthermore, mRNA expression of IL-6 and IL-10 receptors was assessed and intriguingly IL6ST receptor subunit was significantly lower in NBD CSF, but not RRMS while IL10RB was increased in both. Deciphering the role of increased IL-10-producing B cells and IL10RB despite relapsing disease as well as the discordant expression of IL6 and IL6ST may pave the way for a better understanding of the pathophysiology of these neuro-inflammatory disorders. Full article
(This article belongs to the Special Issue B Lymphocytes in Auto-Inflammatory Diseases)
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18 pages, 3393 KiB  
Article
Altered Phenotype and Enhanced Antibody-Producing Ability of Peripheral B Cells in Mice with Cd19-Driven Cre Expression
by Ying Zhao, Sai Zhao, Xiao-Yuan Qin, Ting-Ting He, Miao-Miao Hu, Zheng Gong, Hong-Min Wang, Fang-Yuan Gong, Xiao-Ming Gao and Jun Wang
Cells 2022, 11(4), 700; https://doi.org/10.3390/cells11040700 - 16 Feb 2022
Cited by 4 | Viewed by 5098
Abstract
Given the importance of B lymphocytes in inflammation and immune defense against pathogens, mice transgenic for Cre under the control of Cd19 promoter (Cd19Cre/+ mice) have been widely used to specifically investigate the role of loxP-flanked genes in B cell [...] Read more.
Given the importance of B lymphocytes in inflammation and immune defense against pathogens, mice transgenic for Cre under the control of Cd19 promoter (Cd19Cre/+ mice) have been widely used to specifically investigate the role of loxP-flanked genes in B cell development/function. However, impacts of expression/insertion of the Cre transgene on the phenotype and function of B cells have not been carefully studied. Here, we show that the number of marginal zone B and B1a cells was selectively reduced in Cd19Cre/+ mice, while B cell development in the bone marrow and total numbers of peripheral B cells were comparable between Cd19Cre/+ and wild type C57BL/6 mice. Notably, humoral responses to both T cell-dependent and independent antigens were significantly increased in Cd19Cre/+ mice. We speculate that these differences are mainly attributable to reduced surface CD19 levels caused by integration of the Cre-expressing cassette that inactivates one Cd19 allele. Moreover, our literature survey showed that expression of Cd19Cre/+ alone may affect the development/progression of inflammatory and anti-infectious responses. Thus, our results have important implications for the design and interpretation of results on gene functions specifically targeted in B cells in the Cd19Cre/+ mouse strain, for instance, in the context of (auto) inflammatory/infectious diseases. Full article
(This article belongs to the Special Issue B Lymphocytes in Auto-Inflammatory Diseases)
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7 pages, 1275 KiB  
Article
Type II Collagen-Specific B Cells Induce Immune Tolerance in Th1-Skewed, Th2-Skewed, and Arthritis-Prone Strains of Mice
by Shukkur M. Farooq and Hossam M. Ashour
Cells 2021, 10(4), 870; https://doi.org/10.3390/cells10040870 - 12 Apr 2021
Cited by 4 | Viewed by 2327
Abstract
Antigen-specific regulatory T cells play key immune suppressive roles in autoimmune disease models and regulate the peripheral tolerance achieved via anterior chamber-associated immune deviation (ACAID). Articular cartilage has type II collagen (CII), which is a potent autoantigen protein in arthritis. There has not [...] Read more.
Antigen-specific regulatory T cells play key immune suppressive roles in autoimmune disease models and regulate the peripheral tolerance achieved via anterior chamber-associated immune deviation (ACAID). Articular cartilage has type II collagen (CII), which is a potent autoantigen protein in arthritis. There has not been much research on the clinical importance of CII-associated diseases. Moreover, the capability of CII to induce immune tolerance has not been previously assessed. We reported that delivery of CII either directly into the eye or via intravenous injection of CII-specific ACAID antigen presenting cells (APCs) can induce ACAID. Here, we hypothesized that peripheral tolerance can be induced following adoptive transfer of in vitro generated CII-specific ACAID B cells to naive mice. Delayed hypersensitivity (DTH) assays were used to assess the suppressive ability of adoptively transferred B cells. Immune responses of ACAID B cell-injected mice were significantly suppressed following challenges with CII as compared to positive controls. This effect was replicated in three different strains of mice (C57BL/6, BALB/c, and DBA/1). Thus, CII-specific ACAID B cells were able to induce immune tolerance in Th1-skewed, Th2-skewed, and arthritis-prone mice. ACAID B cell-mediated tolerance induced by CII could have therapeutic implications for the treatment of CII-mediated autoimmune diseases. Full article
(This article belongs to the Special Issue B Lymphocytes in Auto-Inflammatory Diseases)
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Review

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12 pages, 1166 KiB  
Review
B Cells at the Cross-Roads of Autoimmune Diseases and Auto-Inflammatory Syndromes
by Moncef Zouali
Cells 2022, 11(24), 4025; https://doi.org/10.3390/cells11244025 - 12 Dec 2022
Cited by 6 | Viewed by 2529
Abstract
Whereas autoimmune diseases are mediated primarily by T and B cells, auto-inflammatory syndromes (AIFS) involve natural killer cells, macrophages, mast cells, dendritic cells, different granulocyte subsets and complement components. In contrast to autoimmune diseases, the immune response of patients with AIFS is not [...] Read more.
Whereas autoimmune diseases are mediated primarily by T and B cells, auto-inflammatory syndromes (AIFS) involve natural killer cells, macrophages, mast cells, dendritic cells, different granulocyte subsets and complement components. In contrast to autoimmune diseases, the immune response of patients with AIFS is not associated with a breakdown of immune tolerance to self-antigens. Focusing on B lymphocyte subsets, this article offers a fresh perspective on the multiple cross-talks between both branches of innate and adaptive immunity in mounting coordinated signals that lead to AIFS. By virtue of their potential to play a role in adaptive immunity and to exert innate-like functions, B cells can be involved in both promoting inflammation and mitigating auto-inflammation in disorders that include mevalonate kinase deficiency syndrome, Kawasaki syndrome, inflammatory bone disorders, Schnitzler syndrome, Neuro-Behçet’s disease, and neuromyelitis optica spectrum disorder. Since there is a significant overlap between the pathogenic trajectories that culminate in autoimmune diseases, or AIFS, a more detailed understanding of their respective roles in the development of inflammation could lead to designing novel therapeutic avenues. Full article
(This article belongs to the Special Issue B Lymphocytes in Auto-Inflammatory Diseases)
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