Special Issue "B Cells in Autoimmunity"

A special issue of Journal of Clinical Medicine (ISSN 2077-0383). This special issue belongs to the section "Clinical Cytology".

Deadline for manuscript submissions: closed (31 August 2016).

Special Issue Editor

Dr. Bonnie N. Dittel
E-Mail Website
Guest Editor
Blood Research Institute, BloodCenter of Wisconsin, USA
Interests: regulatory B cells; immune-mediated neuronal damage; myeloperoxidase (MPO)

Special Issue Information

Dear Colleagues,

B cells play an important role in the immune response by antigen presentation and cytokine and antibody production. Unfortunately, the same functional attributes of B cells that are indispensable for protection against pathogens can also contribute to the etiology of certain autoimmune diseases. Conversely, several studies also suggest regulatory potential of B cells and highlight their role in controlling autoimmunity. Thus, it is evident that B cells can play a dual role in autoimmune diseases. It is likely that different subsets of B cells are either pathogenic or regulatory in nature. Although an active area of research, it is still not clear when, how and which subsets of B cells play one or the other role in the context of different autoimmune diseases. Of clinical relevance, therapeutic B cell depletion strategies are increasingly being used for the management of some autoimmune diseases. Although, they show efficacy in some clinical trials, adverse autoimmune reactions are also reported in some patients undergoing these therapy. Thus, it is very important to know when and how different subsets of B cells play either a pathogenic or a regulatory role, in the context of different autoimmune diseases, so that they can be precisely targeted for therapeutic purpose. Please join us in presenting this special issue focused on understanding the differential roles and mechanisms of action of different B cell subsets in autoimmunity that would be helpful for developing safe and effective B cell-targeted therapies.

Dr. Bonnie N. Dittel
Dr. Avijit Ray
Guest Editors

Manuscript Submission Information

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Keywords

  • Autoimmunity
  • Autoantibody
  • Pathogenic B cell
  • Regulatory B cell
  • B cell-targeted therapy
  • B cell depletion.

Published Papers (5 papers)

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Research

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Open AccessArticle
B Cell Receptor Affinity for Insulin Dictates Autoantigen Acquisition and B Cell Functionality in Autoimmune Diabetes
J. Clin. Med. 2016, 5(11), 98; https://doi.org/10.3390/jcm5110098 - 08 Nov 2016
Cited by 4
Abstract
B cells have been strongly implicated in the development of human type 1 diabetes and are required for disease in the NOD mouse model. These functions are dependent on B cell antigen receptor (BCR) specificity and expression of MHC, implicating linked autoantigen recognition [...] Read more.
B cells have been strongly implicated in the development of human type 1 diabetes and are required for disease in the NOD mouse model. These functions are dependent on B cell antigen receptor (BCR) specificity and expression of MHC, implicating linked autoantigen recognition and presentation to effector T cells. BCR-antigen affinity requirements for participation in disease are unclear. We hypothesized that BCR affinity for the autoantigen insulin differentially affects lymphocyte functionality, including tolerance modality and the ability to acquire and become activated in the diabetogenic environment. Using combined transgenic and retrogenic heavy and light chain to create multiple insulin-binding BCRs, we demonstrate that affinity for insulin is a critical determinant of the function of these autoreactive cells. We show that both BCR affinity for insulin and genetic background affect tolerance induction in immature B cells. We also find new evidence that may explain the enigmatic ability of B cells expressing 125 anti-insulin BCR to support development of TID in NOD mice despite a reported affinity beneath requirements for binding insulin at in vivo concentrations. We report that when expressed as an antigen receptor the affinity of 125 is much higher than determined by measurements of the soluble form. Finally, we show that in vivo acquisition of insulin requires both sufficient BCR affinity and permissive host/tissue environment. We propose that a confluence of BCR affinity, pancreas environment, and B cell tolerance-regulating genes in the NOD animal allows acquisition of insulin and autoimmunity. Full article
(This article belongs to the Special Issue B Cells in Autoimmunity)
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Review

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Open AccessReview
Mechanisms by Which B Cells and Regulatory T Cells Influence Development of Murine Organ-Specific Autoimmune Diseases
J. Clin. Med. 2017, 6(2), 13; https://doi.org/10.3390/jcm6020013 - 26 Jan 2017
Cited by 9
Abstract
Experiments with B cell-deficient (B−/−) mice indicate that a number of autoimmune diseases require B cells in addition to T cells for their development. Using B−/− Non-obese diabetic (NOD) and NOD.H-2h4 mice, we demonstrated that development of spontaneous autoimmune thyroiditis (SAT), Sjogren’s syndrome [...] Read more.
Experiments with B cell-deficient (B−/−) mice indicate that a number of autoimmune diseases require B cells in addition to T cells for their development. Using B−/− Non-obese diabetic (NOD) and NOD.H-2h4 mice, we demonstrated that development of spontaneous autoimmune thyroiditis (SAT), Sjogren’s syndrome and diabetes do not develop in B−/− mice, whereas all three diseases develop in B cell-positive wild-type (WT) mice. B cells are required early in life, since reconstitution of adult mice with B cells or autoantibodies did not restore their ability to develop disease. B cells function as important antigen presenting cells (APC) to initiate activation of autoreactive CD4+ effector T cells. If B cells are absent or greatly reduced in number, other APC will present the antigen, such that Treg are preferentially activated and effector T cells are not activated. In these situations, B−/− or B cell-depleted mice develop the autoimmune disease when T regulatory cells (Treg) are transiently depleted. This review focuses on how B cells influence Treg activation and function, and briefly considers factors that influence the effectiveness of B cell depletion for treatment of autoimmune diseases. Full article
(This article belongs to the Special Issue B Cells in Autoimmunity)
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Open AccessFeature PaperReview
Mechanisms of Regulatory B cell Function in Autoimmune and Inflammatory Diseases beyond IL-10
J. Clin. Med. 2017, 6(1), 12; https://doi.org/10.3390/jcm6010012 - 23 Jan 2017
Cited by 23
Abstract
In the past two decades it has become clear that in addition to antigen presentation and antibody production B cells play prominent roles in immune regulation. While B cell-derived IL-10 has garnered much attention, B cells also effectively regulate inflammation by a variety [...] Read more.
In the past two decades it has become clear that in addition to antigen presentation and antibody production B cells play prominent roles in immune regulation. While B cell-derived IL-10 has garnered much attention, B cells also effectively regulate inflammation by a variety of IL-10-independent mechanisms. B cell regulation has been studied in both autoimmune and inflammatory diseases. While collectively called regulatory B cells (Breg), no definitive phenotype has emerged for B cells with regulatory potential. This has made their study challenging and thus unique B cell regulatory mechanisms have emerged in a disease-dependent manner. Thus to harness the therapeutic potential of Breg, further studies are needed to understand how they emerge and are induced to evoke their regulatory activities. Full article
(This article belongs to the Special Issue B Cells in Autoimmunity)
Open AccessReview
Inebilizumab, a B Cell-Depleting Anti-CD19 Antibody for the Treatment of Autoimmune Neurological Diseases: Insights from Preclinical Studies
J. Clin. Med. 2016, 5(12), 107; https://doi.org/10.3390/jcm5120107 - 24 Nov 2016
Cited by 15
Abstract
Exaggerated or inappropriate responses by B cells are an important feature in many types of autoimmune neurological diseases. The recent success of B-cell depletion in the treatment of multiple sclerosis (MS) has stimulated the development of novel B-cell-targeting therapies with the potential for [...] Read more.
Exaggerated or inappropriate responses by B cells are an important feature in many types of autoimmune neurological diseases. The recent success of B-cell depletion in the treatment of multiple sclerosis (MS) has stimulated the development of novel B-cell-targeting therapies with the potential for improved efficacy. CD19 has emerged as a promising target for the depletion of B cells as well as CD19-positive plasmablasts and plasma cells. Inebilizumab (MEDI-551), an anti-CD19 antibody with enhanced antibody-dependent cell-mediated cytotoxicity against B cells, is currently being evaluated in MS and neuromyelitis optica. This review discusses the role of B cells in autoimmune neurological disorders, summarizes the development of inebilizumab, and analyzes the recent results for inebilizumab treatment in an autoimmune encephalitis mouse model. The novel insights obtained from these preclinical studies can potentially guide future investigation of inebilizumab in patients. Full article
(This article belongs to the Special Issue B Cells in Autoimmunity)
Open AccessReview
Multiple Roles for B-Lymphocytes in Sjogren’s Syndrome
J. Clin. Med. 2016, 5(10), 87; https://doi.org/10.3390/jcm5100087 - 08 Oct 2016
Cited by 9
Abstract
Sjogren’s syndrome (SS) is a complex heterogeneous autoimmune disease resulting in loss of salivary gland and lacrimal gland function that may include multiple systemic manifestations including lymphoma. Multiple cell types participate in disease pathogenesis. This review discusses evidence for abnormal B cell subpopulations [...] Read more.
Sjogren’s syndrome (SS) is a complex heterogeneous autoimmune disease resulting in loss of salivary gland and lacrimal gland function that may include multiple systemic manifestations including lymphoma. Multiple cell types participate in disease pathogenesis. This review discusses evidence for abnormal B cell subpopulations in patients with SS, critical roles of B cells in SS and the status of B cell–directed therapies in the management of patients with SS. Full article
(This article belongs to the Special Issue B Cells in Autoimmunity)
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