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B Cells and Immunological Tolerance 2.0
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B Cells and Immunological Tolerance 2.0

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Immunology".

Deadline for manuscript submissions: closed (30 November 2021) | Viewed by 27791

Special Issue Editors

Prof. Dr. Marcos López Hoyos

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Guest Editor
1. Immunology Service, University Hospital Marqués de Valdecilla-IDIVAL, 39008 Santander, Spain
2. Molecular Biology Department, Universidad de Cantabria, 39005 Santander, Spain
Interests: immunology; autoimmunity; transplantation; tolerance; human pathology; biomarkers
Special Issues, Collections and Topics in MDPI journals
Dr. Ramón Merino

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Guest Editor
Instituto de Biomedicina y Biotecnología de Cantabria, Consejo Superior de Investigaciones Científicas-Universidad de Cantabria, Molecular Biology Department, Universidad de Cantabria, 39011 Santander, Spain
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue is a continuation of our previous Special Issue "B Cells and Immunological Tolerance".

The main goal of the immune system is to protect the body against foreign agents. To achieve this mission, the immune system acquires an advanced degree of specialization that allows it to recognize and neutralize any pathogen and danger signal present in the organism. The immune response must be capable of being triggered by harmful extraneous stimuli and, once the danger is eliminated, it must be silenced and not perpetuated over time. A failure in the correct shutdown of the immune response may be the basis of many inflammatory processes. On the other hand, this high degree of specialization increases the risk of systemic ruptures of the physiological mechanisms controlling immunological tolerance and anomalous or unanticipated responses are induced, as in the case of autoimmune diseases, where some "misguided" immune cells attack their own antigens (autoantigens). To counter these effects, the immune system has established a balanced equilibrium between the effector and the inhibitor mechanisms of the immune response. This issue focuses on tolerance mechanisms affecting B cell responses from the molecular level (microRNA, microbiota…) to the cellular level (apoptosis, Bregs). These are targets for the development of diagnostic and/or therapeutic approaches in human inflammatory, autoimmune or alloimmune processes.

Dr. Marcos Lopez-Hoyos
Dr. Ramón Merino
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • B cell tolerance
  • autoimmune
  • alloimmune
  • mechanisms
  • diagnostic
  • therapeutics

Related Special Issue

Published Papers (6 papers)

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Research

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13 pages, 2764 KiB  
Article
In Vitro Characterization of Human CD24hiCD38hi Regulatory B Cells Shows CD9 Is Not a Stable Breg Cell Marker
by Fatin N. Mohd Jaya, Sergio G. Garcia, Francesc E. Borras, Dolores Guerrero, Godfrey C. F. Chan and Marcella Franquesa
Int. J. Mol. Sci. 2021, 22(9), 4583; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094583 - 27 Apr 2021
Cited by 5 | Viewed by 2661
Abstract
Regulatory B (Breg) cells are endowed with immune suppressive functions. Various human and murine Breg subtypes have been reported. While interleukin (IL)-10 intracellular staining remains the most reliable way to identify Breg cells, this technique hinders further essential functional studies. Recent findings suggest [...] Read more.
Regulatory B (Breg) cells are endowed with immune suppressive functions. Various human and murine Breg subtypes have been reported. While interleukin (IL)-10 intracellular staining remains the most reliable way to identify Breg cells, this technique hinders further essential functional studies. Recent findings suggest that CD9 is an effective surface marker of murine IL-10 competent Breg cells. However, the stability of CD9 and its relevance as a unique marker for human Breg cells, which have been widely characterized as CD24hiCD38hi, have not been investigated. Here, we demonstrate that CD9 expression is sensitive to in vitro B cell stimulations. CD9 expression could either be re-expressed or downregulated in purified CD9-negative B cells and CD9-positive B cells, respectively. We found no significant differences in the Breg differentiation capacity of the CD9-negative and CD9-positive B cells. Furthermore, CD9-positive B cells co-express CD40 and CD86, suggesting their nature as B cell activation or co-stimulatory molecules, rather than regulatory ones. Therefore, we report the relatively unstable CD9 as a distinct surface molecule, indicating the need for further research for a more reliable marker to purify human Breg cells. Full article
(This article belongs to the Special Issue B Cells and Immunological Tolerance 2.0)
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14 pages, 3303 KiB  
Article
A Germline-Encoded Structural Arginine Trap Underlies the Anti-DNA Reactivity of a Murine V Gene Segment
by Ronny Petterson dos Santos Araújo, Renato Kaylan Alves França, Napoleão Fonseca Valadares, Andrea Queiroz Maranhão and Marcelo Macedo Brigido
Int. J. Mol. Sci. 2021, 22(9), 4541; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094541 - 26 Apr 2021
Cited by 1 | Viewed by 2081
Abstract
Autoimmunity may have its origins of early repertoire selection in developmental B cells. Such a primary repertoire is probably shaped by selecting B cells that can efficiently perform productive signaling, stimulated by self-antigens in the bone marrow, such as DNA. In support of [...] Read more.
Autoimmunity may have its origins of early repertoire selection in developmental B cells. Such a primary repertoire is probably shaped by selecting B cells that can efficiently perform productive signaling, stimulated by self-antigens in the bone marrow, such as DNA. In support of that idea, we previously found a V segment from VH10 family that can form antibodies that bind to DNA independent of CDR3 usage. In this paper we designed four antibody fragments in a novel single-chain pre-BCR (scpre-BCR) format containing germinal V gene segments from families known to bind DNA (VH10) or not (VH4) connected to a murine surrogate light chain (SLC), lacking the highly charged unique region (UR), by a hydrophilic peptide linker. We also tested the influence of CDR2 on DNA reactivity by shuffling the CDR2 loop. The scpre-BCRs were expressed in bacteria. VH10 bearing scpre-BCR could bind DNA, while scpre-BCR carrying the VH4 segment did not. The CDR2 loop shuffling hampered VH10 reactivity while displaying a gain-of-function in the nonbinding VH4 germline. We modeled the binding sites demonstrating the conservation of a positivity charged pocket in the VH10 CDR2 as the possible cross-reactive structural element. We presented evidence of DNA reactivity hardwired in a V gene, suggesting a structural mechanism for innate autoreactivity. Therefore, while autoreactivity to DNA can lead to autoimmunity, efficiently signaling for B cell development is likely a trade-off mechanism leading to the selection of potentially autoreactive repertoires. Full article
(This article belongs to the Special Issue B Cells and Immunological Tolerance 2.0)
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Review

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22 pages, 1470 KiB  
Review
Marginal Zone B-Cell Populations and Their Regulatory Potential in the Context of HIV and Other Chronic Inflammatory Conditions
by Kim Doyon-Laliberté, Matheus Aranguren, Johanne Poudrier and Michel Roger
Int. J. Mol. Sci. 2022, 23(6), 3372; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms23063372 - 21 Mar 2022
Cited by 7 | Viewed by 5266
Abstract
Inflammation in the context of Human Immunodeficiency Virus (HIV) establishes early and persists beyond antiretroviral therapy (ART). As such, we have shown excess B-cell activating factor (BAFF) in the blood of HIV-infected progressors, as soon as in the acute phase, and despite successful [...] Read more.
Inflammation in the context of Human Immunodeficiency Virus (HIV) establishes early and persists beyond antiretroviral therapy (ART). As such, we have shown excess B-cell activating factor (BAFF) in the blood of HIV-infected progressors, as soon as in the acute phase, and despite successful ART. Excess BAFF was associated with deregulation of the B-cell compartment; notably, with increased frequencies of a population sharing features of both transitional immature (TI) and marginal zone (MZ) B-cells, we termed Marginal Zone precursor-like (MZp). We have reported similar observations with HIV-transgenic mice, Simian Immunodeficiency Virus (SIV)-infected macaques, and more recently, with HIV-infected Beninese commercial sex workers, which suggests that excess BAFF and increased frequencies of MZp B-cells are reliable markers of inflammation in the context of HIV. Importantly, we have recently shown that in healthy individuals, MZps present an important regulatory B-cell (Breg) profile and function. Herein, we wish to review our current knowledge on MZ B-cell populations, especially their Breg status, and that of other B-cell populations sharing similar features. BAFF and its analog A Proliferation-Inducing Ligand (APRIL) are important in shaping the MZ B-cell pool; moreover, the impact that excess BAFF—encountered in the context of HIV and several chronic inflammatory conditions—may exert on MZ B-cell populations, Breg and antibody producing capacities is a threat to the self-integrity of their antibody responses and immune surveillance functions. As such, deregulations of MZ B-cell populations contribute to autoimmune manifestations and the development of MZ lymphomas (MZLs) in the context of HIV and other inflammatory diseases. Therefore, further comprehending the mechanisms regulating MZ B-cell populations and their functions could be beneficial to innovative therapeutic avenues that could be deployed to restore MZ B-cell immune competence in the context of chronic inflammation involving excess BAFF. Full article
(This article belongs to the Special Issue B Cells and Immunological Tolerance 2.0)
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19 pages, 1196 KiB  
Review
B Cells in Primary Membranous Nephropathy: Escape from Immune Tolerance and Implications for Patient Management
by Benjamin Y. F. So, Desmond Y. H. Yap and Tak Mao Chan
Int. J. Mol. Sci. 2021, 22(24), 13560; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms222413560 - 17 Dec 2021
Cited by 11 | Viewed by 5778
Abstract
Membranous nephropathy (MN) is an important cause of nephrotic syndrome and chronic kidney disease (CKD) in adults. The pathogenic significance of B cells in MN is increasingly recognized, especially following the discovery of various autoantibodies that target specific podocytic antigens and the promising [...] Read more.
Membranous nephropathy (MN) is an important cause of nephrotic syndrome and chronic kidney disease (CKD) in adults. The pathogenic significance of B cells in MN is increasingly recognized, especially following the discovery of various autoantibodies that target specific podocytic antigens and the promising treatment responses seen with B cell depleting therapies. The presence of autoreactive B cells and autoantibodies that bind to antigens on podocyte surfaces are characteristic features of MN, and are the result of breaches in central and peripheral tolerance of B lymphocytes. These perturbations in B cell tolerance include altered B lymphocyte subsets, dysregulation of genes that govern immunoglobulin production, aberrant somatic hypermutation and co-stimulatory signalling, abnormal expression of B cell-related cytokines, and increased B cell infiltrates and organized tertiary lymphoid structures within the kidneys. An understanding of the role of B cell tolerance and homeostasis may have important implications for patient management in MN, as conventional immunosuppressive treatments and novel B cell-targeted therapies show distinct effects on proliferation, differentiation and reconstitution in different B cell subsets. Circulating B lymphocytes and related cytokines may serve as potential biomarkers for treatment selection, monitoring of therapeutic response and prediction of disease relapse. These recent advances in the understanding of B cell tolerance in MN have provided greater insight into its immunopathogenesis and potential novel strategies for disease monitoring and treatment. Full article
(This article belongs to the Special Issue B Cells and Immunological Tolerance 2.0)
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19 pages, 961 KiB  
Review
B Cells and Microbiota in Autoimmunity
by María Botía-Sánchez, Marta E. Alarcón-Riquelme and Georgina Galicia
Int. J. Mol. Sci. 2021, 22(9), 4846; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms22094846 - 03 May 2021
Cited by 12 | Viewed by 4473
Abstract
Trillions of microorganisms inhabit the mucosal membranes maintaining a symbiotic relationship with the host’s immune system. B cells are key players in this relationship because activated and differentiated B cells produce secretory immunoglobulin A (sIgA), which binds commensals to preserve a healthy microbial [...] Read more.
Trillions of microorganisms inhabit the mucosal membranes maintaining a symbiotic relationship with the host’s immune system. B cells are key players in this relationship because activated and differentiated B cells produce secretory immunoglobulin A (sIgA), which binds commensals to preserve a healthy microbial ecosystem. Mounting evidence shows that changes in the function and composition of the gut microbiota are associated with several autoimmune diseases suggesting that an imbalanced or dysbiotic microbiota contributes to autoimmune inflammation. Bacteria within the gut mucosa may modulate autoimmune inflammation through different mechanisms from commensals ability to induce B-cell clones that cross-react with host antigens or through regulation of B-cell subsets’ capacity to produce cytokines. Commensal signals in the gut instigate the differentiation of IL-10 producing B cells and IL-10 producing IgA+ plasma cells that recirculate and exert regulatory functions. While the origin of the dysbiosis in autoimmunity is unclear, compelling evidence shows that specific species have a remarkable influence in shaping the inflammatory immune response. Further insight is necessary to dissect the complex interaction between microorganisms, genes, and the immune system. In this review, we will discuss the bidirectional interaction between commensals and B-cell responses in the context of autoimmune inflammation. Full article
(This article belongs to the Special Issue B Cells and Immunological Tolerance 2.0)
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15 pages, 651 KiB  
Review
Secretory IgA in Intestinal Mucosal Secretions as an Adaptive Barrier against Microbial Cells
by Bernadeta Pietrzak, Katarzyna Tomela, Agnieszka Olejnik-Schmidt, Andrzej Mackiewicz and Marcin Schmidt
Int. J. Mol. Sci. 2020, 21(23), 9254; https://0-doi-org.brum.beds.ac.uk/10.3390/ijms21239254 - 04 Dec 2020
Cited by 106 | Viewed by 6847
Abstract
Secretory IgA (SIgA) is the dominant antibody class in mucosal secretions. The majority of plasma cells producing IgA are located within mucosal membranes lining the intestines. SIgA protects against the adhesion of pathogens and their penetration into the intestinal barrier. Moreover, SIgA regulates [...] Read more.
Secretory IgA (SIgA) is the dominant antibody class in mucosal secretions. The majority of plasma cells producing IgA are located within mucosal membranes lining the intestines. SIgA protects against the adhesion of pathogens and their penetration into the intestinal barrier. Moreover, SIgA regulates gut microbiota composition and provides intestinal homeostasis. In this review, we present mechanisms of SIgA generation: T cell-dependent and -independent; in different non-organized and organized lymphoid structures in intestinal lamina propria (i.e., Peyer’s patches and isolated lymphoid follicles). We also summarize recent advances in understanding of SIgA functions in intestinal mucosal secretions with focus on its role in regulating gut microbiota composition and generation of tolerogenic responses toward its members. Full article
(This article belongs to the Special Issue B Cells and Immunological Tolerance 2.0)
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