Source: https://www.nature.com/articles/s41581-018-0074-7?error=cookies_not_supported&code=afd8acaf-c790-4faf-b15a-5399c5c08a4b
Timestamp: 2019-04-23 06:34:46+00:00

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B cells have a central role in many autoimmune diseases, including in those with renal involvement, as well as in the immunological response to kidney transplantation. The majority of B cell studies have focused on their pathological role as antibody producers. However, these cells have broad functions in immune responses beyond immunoglobulin secretion, including antigen presentation to T cells and cytokine production. Importantly, not all B cell subsets enhance immune responses. Regulatory B (Breg) cells attenuate inflammation and contribute to the maintenance of immune tolerance. Breg cells are numerically deficient and/or dysfunctional in several autoimmune diseases that can affect the kidneys, including systemic lupus erythematosus and anti-neutrophil cytoplasmic antibody-associated vasculitis, as well as in some groups of renal transplant recipients with alloimmune graft damage. B cell-targeting biologics have been trialled with promising results in diverse immune-mediated renal conditions. These therapies can affect both pro-inflammatory B cells and Breg cells, potentially limiting their long-term efficacy. Future strategies might involve the modulation of pro-inflammatory B cells in combination with the stimulation of regulatory subsets. Additionally, the monitoring of individual B cell subsets in patients may lead to the discovery of novel biomarkers that could help to predict disease relapse or progression.
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A.D.S. is supported by Kidney Research UK.
Nature Reviews Nephrology thanks S. Hillion and the other anonymous reviewer(s) for their contribution to the peer review of this work.
All authors contributed to researching data for the article, discussing the article’s content, writing the article and reviewing and editing the manuscript before submission.
Correspondence to Alan D. Salama.
A triad of symptoms, namely oedema, proteinuria >3.5 g/day and hypoalbuminaemia, which result from glomerular podocyte damage. Patients often present with marked hypercholesterolaemia.
A common cause of nephrotic syndrome in children and adults, which is characterized by minimal histological abnormalities visible by light microscopy, but in which podocyte effacement can be observed by electron microscopy.
A glomerular disease that is characterized by subepithelial immune complexes, which cause nephrotic syndrome and is frequently associated with the presence of autoantibodies to phospholipase A2 receptor or thrombospondin type 1 domain-containing protein 7A.
The initial immunosuppressive therapy used at the time of transplantation or the initial therapy used to treat autoimmune diseases.
The process through which high-affinity, class-switched plasma cells and memory B cells are generated.
An immune response in which mainly T helper 1 (TH1) cells produce cytokines, such as IFNγ and IL-12.
An immune response in which mainly T helper 2 (TH2) cells produce cytokines, such as IL-4.
Organized lymphoid structures that develop in non-lymphoid tissues.
(iNKT cell). A CD1d-restricted T cell that expresses a semi-invariant T cell receptor and recognizes lipid antigens.
Long-term allograft acceptance without the requirement for continuous immunosuppression.
Continuous immunosuppression to maintain stable graft function or remission in cases of autoimmunity.
A syndrome of circulating cryoglobulins, which are immunoglobulins that precipitate at temperatures below 37oC, leading to skin, kidney and neurological disease.

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