B-cell oligoclonal expansions in renal tissue of patients with immune-mediated glomerular disease

Kolovou, Kyriaki; Laskari, Katerina; Roumelioti, Maria; Tektonidou, Maria G; Panayiotidis, Panayiotis; Boletis, John; Marinaki, Smaragdi; Sfikakis, Petros P.

doi:10.1016/j.clim.2020.108488

Cited by 11 publications

(8 citation statements)

References 30 publications

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“…Numbers of plasma cells and regulatory B cells were statistically higher in patients with MN compared with healthy individuals or individuals with non-immune kidney disease and the amount of in vitro-expanded PLA2R-specific memory B cells could be correlated with circulating PLA2R antibody titres 89 . The specific site at which the immune response to PLA2R is initiated remains speculative 90 but intrarenal B cells in tertiary lymphoid follicles have been noted 91,92 . These tertiary follicles could represent the propagation of the immune response triggered by PLA2R shed from podocytes as exosomes into the tubular lumen 93 and later captured by intrarenal dendritic cells.…”

Section: Autoimmune Reactionsmentioning

confidence: 99%

Membranous nephropathy

Ronco

Beck

Dębiec

et al. 2021

Nat Rev Dis Primers

253

167

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Section: Autoimmune Reactionsmentioning

confidence: 99%

Membranous nephropathy

Ronco

Beck

Dębiec

et al. 2021

Nat Rev Dis Primers

253

167

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“…For example, local autoantibodies were produced in patients with rheumatoid arthritis (136). A recent study by Kyriaki Kolovou et al has shown that there is localized B cell infiltration in the kidney in renal diseases characterized by podocyte injury, including membranous nephropathy (137). Huimin Li et al found infiltrating IL-17+ cells in the renal tubule of IMN patients (138).…”

Section: Th Cells Involved In the Immune Dysregulation Of Imnmentioning

confidence: 99%

“…A recent study by Kyriaki Kolovou et al. has shown that there is localized B cell infiltration in the kidney in renal diseases characterized by podocyte injury, including membranous nephropathy ( 137 ). Huimin Li et al.…”

Section: Helper T Cells In Imnmentioning

confidence: 99%

Helper T Cells in Idiopathic Membranous Nephropathy

et al. 2021

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Idiopathic membranous nephropathy (IMN) is an autoimmune disease in which the immune system produces an antibody response to its own antigens due to impaired immune tolerance. Although antibodies are derived from plasma cells differentiated by B cells, the T-B cells also contribute a lot to the immune system. In particular, the subsets of helper T (Th) cells, including the dominant subsets such as Th2, Th17, and follicular helper T (Tfh) cells and the inferior subsets such as regulatory T (Treg) cells, shape the immune imbalance of IMN and promote the incidence and development of autoimmune responses. After reviewing the physiological knowledge of various subpopulations of Th cells and combining the existing studies on Th cells in IMN, the role model of Th cells in IMN was explained in this review. Finally, the existing clinical treatment regimens for IMN were reviewed, and the importance of the therapy for Th cells was highlighted.

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“…This is supported by a clonal analysis of the B cell repertoire in immune-mediated glomerular diseases, which suggests the presence of an antigen-specific process of SHM and CSR that occurs locally in the renal parenchyma. Intrarenal oligoclonal B cells were found in glomerular diseases characterized by podocyte injury, including focal segmental glomerulosclerosis and MN, in the absence of B cell oligoclonality in the peripheral blood [123]. Furthermore, T cell interstitial infiltrates in MN usually show an elevated CD4 + /CD8 + ratio [116]; and in human and experimental models of MN, the Th2 polarization of CD4 + T cells stimulates both peripheral and intrarenal B cells to produce IgG4, the culprit Ig isotype in MN [124].…”

Section: Infiltrating B Cell Subsets and Intrarenal Tertiary Lymphoid...mentioning

confidence: 99%

B Cells in Primary Membranous Nephropathy: Escape from Immune Tolerance and Implications for Patient Management

Yap

Chan

2021

IJMS

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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.

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B-cell oligoclonal expansions in renal tissue of patients with immune-mediated glomerular disease

Cited by 11 publications

References 30 publications

Membranous nephropathy

Membranous nephropathy

Helper T Cells in Idiopathic Membranous Nephropathy

B Cells in Primary Membranous Nephropathy: Escape from Immune Tolerance and Implications for Patient Management

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