Regulatory B cells: The new "It" cell

ArticleinTransplantation Proceedings 46(1) · November 2013with31 Reads
DOI: 10.1016/j.transproceed.2013.08.075 · Source: PubMed
Regulatory B cells (Breg) are a subpopulation of B cells that play a suppressive role in the immune system. The mechanism of how these immune cells perform their effects has been explored by experiments in mice and in humans. Intracellular staining for interleukin 10 continues to be a consistent and reproducible method of identifying Breg in mouse and human studies. The lack of Breg is associated with a worsening of several autoimmune diseases such as collagen-induced arthritis, systemic lupus erythematosus, and experimental autoimmune encephalomyelitis in murine studies. The purpose of this review is to provide a concise summary of the role of Breg in the immune system, including the most recently studied cell surface markers associated with Breg, and to describe the role of Breg in the etiology of several autoimmune diseases, the current understanding of Breg development, their role in the development of autoimmune diseases, and their role in inducing tolerance after transplantation.
    • "Bregs are being increasingly recognised as a crucial player in the maintenance of Intestinal homeostasis as they provide a response to dysbiosis which is as effective but more rapid than that achieved by changes in the numbers and activity of Tregs [82]. It is therefore unsurprising that the role of this subset in the prevention and genesis of autoimmunity is an area of expanding research (reviewed in [83]. The importance of B cells in compensatory cross talk between the host and disturbances in the composition of the microbiota is further illustrated by the role of activated B and Plasma cells in the LP and PP in maintaining homeostasis [84]. "
    [Show abstract] [Hide abstract] ABSTRACT: BACKGROUND: In steady state conditions intestinal immune homeostasis is maintained by a sophisticated bidirectional dialogue between the microbiota and the intestinal immune system. This "cross talk" is enabled by the presence of highly adapted secretory cells, sampling cells and pattern recognition receptors in the gastric epithelium. METHODS: Herein we discuss the mechanisms involved in the breakdown of intestinal homeostasis and the development of systemic immune activation and neuroinflammation with a view to discussing the importance of these processes, in tandem with genetic and environmental factors, in the pathophysiology of (auto)immune diseases.Data is presented explaining how immune tolerance is maintained and how it may breakdown. CONCLUSIONS: The breakdown of immune homeostasis following the development of gut inflammation, caused for example by gut dysbiosis, and the consequent increased intestinal permeability, is increasingly considered to be the ultimate source of the systemic immune activation and T helper 17/T regulatory cell imbalances, and maybe neurological disturbances, seen in autoimmune diseases such as Type 1 diabetes and inflammatory bowel disease. Increased intestinal permeability and translocation of commensal antigens into the systemic circulation is also a likely cause of the severe fatigue and an almost bewildering range of neurocognitive, neuroimaging and overall symptom presentations seen in patients with a diagnosis of Chronic Fatigue Syndrome.
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    • "Very recently, a new subset of B lymphocytes has been described, endowed with immunosuppressive activity and so referred as regulatory B cells or simply as ''B reg''. The main function of regulatory B cells is the production of IL- 10, so that the intracellular staining for this cytokine is currently the main method for identifying these cells, even if the recently described B population CD24highCD27?? probably include the large proportion of human Breg [89, 90]. The immunosuppressive properties of IL-10 are well established in animal models of collagen-induced arthritis and experimental autoimmune encephalitis; however, the function of IL-10 in SLE has been very controversial [91, 92]. "
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  • [Show abstract] [Hide abstract] ABSTRACT: Gene replacement therapies, like organ and cell transplantation are likely to introduce neo-antigens that elicit rejection via humoral and/or effector T cell immune responses. Nonetheless, thanks to an ever growing body of pre-clinical studies it is now well accepted that gene transfer protocols can be specifically designed and optimized for induction of antigen-specific immune tolerance. One approach is to specifically express a gene in a tissue with a tolerogenic microenvironment such as the liver or thymus. Another strategy is to transfer a particular gene into hematopoietic stem cells or immunological precursor cells thus educating the immune system to recognize the therapeutic protein as "self". In addition, expression of the therapeutic protein in pro-tolerogenic antigen presenting cells such as immature dendritic cells and B cells has proven to be promising. All three approaches have successfully prevented unwanted immune responses in pre-clinical studies aimed at the treatment of inherited protein deficiencies, e.g. lysosomal storage disorders and hemophilia, and of type I diabetes and multiple sclerosis. In this review we focus on current gene transfer protocols that induce tolerance, including gene delivery vehicles and target tissues, and discuss successes and obstacles in different disease models.
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