Figure 2 Prevention of antigen–antibody

Slides:

Advertisements

Similar presentations

Causes of membranous nephropathy 신장내과 R 3 김경엽. Membranous nephropathy and focal glomerulosclerosis –Most common causes of the nephrotic syndrome in nondiabetic.

Advertisements

Figure 1 Schematic representation of idiopathic nephrotic syndrome,

Laurence H. Beck, Jr. , M. D. , Ph. D. , Ramon G. B. Bonegio, M. D

Figure 1 CTLA-4 and PD-1–PD-L1 immune checkpoints

Figure 2 Cell-mediated disease mechanisms of lupus nephritis

Nat. Rev. Nephrol. doi: /nrneph

Figure 6 Effects of adiponectin on podocyte function

Figure 1 Pre-eclampsia prevents VEGF signalling in endothelial cells

Figure 4 Expression of coagulation protease receptors in renal cells

Volume 82, Issue 7, Pages (October 2012)

Figure 1 Mechanisms of kidney injury in the setting of obesity

Figure 2 Physiological changes in the renal system in pregnancy

Volume 82, Issue 2, Pages (July 2012)

ANCA Associated Vasculitis Secondary to Levamisole-Adultered Cocaine with Associated Membranous Nephropathy: A Case Series Collister et al. Am J Nephrol.

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 Proposed mechanisms underlying the links

Figure 1 Pathways of complement activation

Figure 2 Overview of the complement system

Paraneoplastic glomerulopathies: New insights into an old entity

Figure 3 Putative actions of glucagon-like peptide 1 (GLP-1)

Nat. Rev. Nephrol. doi: /nrneph

Figure 2 Expression of complement activation products in renal samples

Figure 1 Targets for monoclonal antibodies in B-cell lineages

Figure 2 The network of chronic diseases and their mutual influences

Figure 2 Three distinct mechanisms of activation of

Figure 2 Glomerular pathology in mice and humans with diabetic nephropathy Figure 2 | Glomerular pathology in mice and humans with diabetic nephropathy.

Nat. Rev. Nephrol. doi: /nrneph

Figure 2 Podocyte dysfunction is a common feature of renal injury

Figure 5 Comparison of outcomes with belimumab or rituximab therapy

Figure 1 CAR-T-cell design

Nat. Rev. Rheumatol. doi: /nrrheum

Figure 4 Model of changes in the serum levels

Nat. Rev. Nephrol. doi: /nrneph

Volume 82, Issue 7, Pages (October 2012)

Nat. Rev. Nephrol. doi: /nrneph

Figure 2 Emerging models of antibody-mediated rejection (ABMR) and

Figure 4 The molecular configuration of the CD20 molecule

Figure 3 Therapeutic intervention in the complement cascade

Figure 1 Glomerular injury in lupus nephritis

Figure 1 Neuromuscular junction in myasthenia gravis (MG)

Nat. Rev. Nephrol. doi: /nrneph

Figure 3 Localization of ErbB receptors and ligands within the nephron

Figure 3 LDL autoimmunity in atherosclerosis

Nat. Rev. Urol. doi: /nrurol

Nat. Rev. Nephrol. doi: /nrneph

during the alloimmune response

Complement in Kidney Disease: Core Curriculum 2015

Figure 4 Podocyte–endothelial cross talk and activation of heparanase

Figure 3 Pathological activation of complement

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 Identification of anti-HLA antibodies

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Nephrol. doi: /nrneph

Nat. Rev. Endocrinol. doi: /nrendo

Nat. Rev. Nephrol. doi: /nrneph

Figure 1 The major pathways of lipid metabolism

Figure 2 Biologics that target CD4+ T helper (TH)-cell subsets

Figure 4 The complement drug development pipeline

Figure 1 Sequence of events in the development of autoimmune nephritis

Complement in Kidney Disease: Core Curriculum 2015

AJKD Atlas of Renal Pathology: Membranous Nephropathy

A personal hypothetical mechanistic interpretation of idiopathic MN

Simplified diagrammatic representation of a selection of mechanisms of glomerular injury. Simplified diagrammatic representation of a selection of mechanisms.

Antibody-guided diagnosis and treatment algorithm for primary membranous nephropathy (PMN). Antibody-guided diagnosis and treatment algorithm for primary.

Conditions within the kidney that are conducive to C activation.

Membranous nephropathy: recent travels and new roads ahead

Immunofluorescence microscopy in primary membranous nephropathy (PMN).

Pathogenesis of minimal change disease: hypotheses.

Electron micrograph of chronic primary membranous nephropathy showing discontinuous, electron-dense deposits representing aggregates of PLA2R–anti-PLA2R.

Presentation transcript:

Figure 2 Prevention of antigen–antibody immunocomplex deposition on the glomerular basement membrane Figure 2 | Prevention of antigen–antibody immunocomplex deposition on the glomerular basement membrane. a | A glomerular capillary and its basement membrane surrounded by podocytes. Anti-M-type phospholipase A2 receptor (PLA2R) antibodies are shown in the capillary lumen. b | Binding of circulating anti PLA2R autoantibodies to their specific cystein-rich domain (CysR), C-type lectin domain (CTLD)1 or CTLD7 epitopes expressed by the PLA2R receptor on the podocyte cell surface leads to the deposition of antigen–antibody subepithelial immunocomplexes that activate the complement system with secondary podocyte damage and proteinuria. In theory, antibody–antigen binding and the deposition of subepithelial immunocomplexes could be prevented by epitope-specific ligands that bind circulating antiPLA2R antibodies and prevent their binding to epitopes of the PLA2R antigen. Ruggenenti, P. et al. (2017) Treatment of membranous nephropathy: time for a paradigm shift Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.92