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    18. Immune-mediated renal disease. Cunard Robyn,Kelly Carolyn J The Journal of allergy and clinical immunology Immune-mediated renal diseases can be classified by the clinical syndromes they produce, by the attendant renal pathology, or by the dominant immune effector mechanism of renal injury. The major clinical syndromes produced by immune-mediated renal injury include the nephrotic syndrome, the nephritic syndrome, rapidly progressive glomerulonephritis, and acute renal failure. The notion of clinical syndromes facilitates diagnosis and treatment, but does not accurately define disease pathogenesis. In this summary, we discuss pathologically defined immune-mediated renal diseases under the clinical syndrome with which they are most frequently associated. There is overlap between the clinical syndromes, but the syndromes provide a useful framework. Relevant information regarding the proposed pathogenesis of disease entities is included under specific disease entities. 10.1067/mai.2003.126
    Regulatory T cells in immune-mediated renal disease. Ghali Joanna R,Wang Yuan Min,Holdsworth Stephen R,Kitching A Richard Nephrology (Carlton, Vic.) Regulatory T cells (Tregs) are CD4+ T cells that can suppress immune responses by effector T cells, B cells and innate immune cells. This review discusses the role that Tregs play in murine models of immune-mediated renal diseases and acute kidney injury and in human autoimmune kidney disease (such as systemic lupus erythematosus, anti-glomerular basement membrane disease, anti-neutrophil cytoplasmic antibody-associated vasculitis). Current research suggests that Tregs may be reduced in number and/or have impaired regulatory function in these diseases. Tregs possess several mechanisms by which they can limit renal and systemic inflammatory immune responses. Potential therapeutic applications involving Tregs include in vivo induction of Tregs or inducing Tregs from naïve CD4+ T cells or expanding natural Tregs ex vivo, to use as a cellular therapy. At present, the optimal method of generating a phenotypically stable pool of Tregs with long-lasting suppressive effects is not established, but human studies in renal transplantation are underway exploring the therapeutic potential of Tregs as a cellular therapy, and if successful may have a role as a novel therapy in immune-mediated renal diseases. 10.1111/nep.12574
    Immune-mediated kidney disease in 2017: Progress in mechanisms and therapy for immunological kidney disease. Holdsworth Stephen R,Kitching A Richard Nature reviews. Nephrology 10.1038/nrneph.2017.171
    Pathogenic T-Cell Responses in Immune-Mediated Glomerulonephritis. Cells Glomerulonephritis (GN) comprises a group of immune-mediated kidney diseases affecting glomeruli and the tubulointerstitium. Glomerular crescent formation is a histopathological characteristic of severe forms of GN, also referred to as crescentic GN (cGN). Based on histological findings, cGN includes anti-neutrophil cytoplasmic antibody (ANCA)-associated GN, a severe form of ANCA-associated vasculitis, lupus nephritis associated with systemic lupus erythematosus, Goodpasture's disease, and IgA nephropathy. The immunopathogenesis of cGN is associated with activation of CD4 and CD8 T cells, which particularly accumulate in the periglomerular and tubulointerstitial space but also infiltrate glomeruli. Clinical observations and functional studies in pre-clinical animal models provide evidence for a pathogenic role of Th1 and Th17 cell-mediated immune responses in cGN. Emerging evidence further argues that CD8 T cells have a role in disease pathology and the mechanisms of activation and function of recently identified tissue-resident CD4 and CD8 T cells in cGN are currently under investigation. This review summarizes the mechanisms of pathogenic T-cell responses leading to glomerular damage and renal inflammation in cGN. Advanced knowledge of the underlying immune mechanisms involved with cGN will enable the identification of novel therapeutic targets for the replacement or reduction in standard immunosuppressive therapy or the treatment of refractory disease. 10.3390/cells11101625
    Effector and regulatory B cells in immune-mediated kidney disease. Nature reviews. Nephrology 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 (B) cells attenuate inflammation and contribute to the maintenance of immune tolerance. B 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 B 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. 10.1038/s41581-018-0074-7
    [Pathogenesis of immune glomerulonephritis]. Rougier Jean-Philippe,Ronco Pierre La Revue du praticien Immune glomerulonephritis (GN) initially develop as a result of inappropriate immune response, either inadequately directed to self-antigens, or unable to effectively eliminate a foreign antigen. This abnormal immune response leads to the formation of circulating immune complexes, auto-antibodies or self-reactive effector T cells that target glomerular antigens or to the inappropriate regulation of IgA producing lymphocytes (Berger disease) or helper T lymphocyte sub populations (minimal change nephrotic syndrome). In most of the cases, the initial immune injury induces an inflammatory response. However, it is the extent of the interstitial fibrosis which is genetically controlled, that conditioned the evolution of the initial glomerular injury to glomerular sclerosis and progressive renal failure. Recent data on the pathogenesis of the most frequent GN are reported: IgA nephropathy, membranous nephropathy and minimal change nephrotic syndrome. Recent significant advances in the pathophysiology of those glomerular diseases have shed considerable light on the understanding of the underlying disease even if they do not have immediate therapeutic implications.
    Advances in Understanding of Pathogenesis and Treatment of Immune-Mediated Kidney Disease: A Review. Kant Sam,Kronbichler Andreas,Sharma Purva,Geetha Duvuru American journal of kidney diseases : the official journal of the National Kidney Foundation There continues to be rapid advancement in our understanding of the pathogenesis of immune-mediated kidney disease. This progress has culminated in the development of multiple therapeutic agents that have consistently improved renal and patient outcomes. The focus of this review is to discuss these recent advancements in immune-mediated kidney disease via the lens of direct and indirect immune-mediated mechanisms. In the direct immune-mediated disease, recently described antigens in anti-glomerular basement membrane (GBM) disease and membranous nephropathy are discussed, along with new therapeutic regimens in membranous nephropathy and focal segmental glomerulosclerosis. From an indirect immune-mediated disease standpoint, recent pivotal trials in antineutrophil cytoplasmic antibody vasculitis, lupus nephritis, and IgA nephropathy are examined from a real-world practice perspective. New molecular pathways in various disorders of alternate complement pathway are described, which in turn have led to development of various experimental therapies. In addition, pivotal and ongoing therapeutic trials in the aforementioned diseases are presented. 10.1053/j.ajkd.2021.07.019