T cell mediated autoimmune glomerular disease in mice

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Abstract

Many forms of glomerulonephritis are mediated by autoimmunity. While autoantibodies are often pathogenic, cell-mediated immunity plays an important role in a number of forms of rapidly progressive glomerulonephritis. This unit describes the induction of cell-mediated autoimmune glomerular disease in mice. One disease model, experimental anti-glomerular basement membrane (GBM) disease, features autoreactivity to a well-defined component of type IV collagen found in the GBM, alpha3(IV)NC1. The other models the cell-mediated effector response in forms of renal vasculitis, where autoantibodies to myeloperoxidase result in systemic neutrophil activation, resulting in their localization to the glomerulus and the subsequent deposition of myeloperoxidase within glomerular capillaries. There, myeloperoxidase acts as a planted autoantigen and is recognized by effector autoreactive myeloperoxidase-specific T cells. These models are useful both in defining mechanisms germane to the development of autoimmunity to alpha3(IV)NC1 and myeloperoxidase, and in dissecting the role of cell-mediated responses in effecting glomerular injury. (c) 2014 by John Wiley Sons, Inc.
Original languageEnglish
Pages (from-to)1 - 19
Number of pages19
JournalCurrent Protocols in Immunology
Volume107
DOIs
Publication statusPublished - 2014

Cite this

@article{50c8013ada0641f98607ab9afa7e48de,
title = "T cell mediated autoimmune glomerular disease in mice",
abstract = "Many forms of glomerulonephritis are mediated by autoimmunity. While autoantibodies are often pathogenic, cell-mediated immunity plays an important role in a number of forms of rapidly progressive glomerulonephritis. This unit describes the induction of cell-mediated autoimmune glomerular disease in mice. One disease model, experimental anti-glomerular basement membrane (GBM) disease, features autoreactivity to a well-defined component of type IV collagen found in the GBM, alpha3(IV)NC1. The other models the cell-mediated effector response in forms of renal vasculitis, where autoantibodies to myeloperoxidase result in systemic neutrophil activation, resulting in their localization to the glomerulus and the subsequent deposition of myeloperoxidase within glomerular capillaries. There, myeloperoxidase acts as a planted autoantigen and is recognized by effector autoreactive myeloperoxidase-specific T cells. These models are useful both in defining mechanisms germane to the development of autoimmunity to alpha3(IV)NC1 and myeloperoxidase, and in dissecting the role of cell-mediated responses in effecting glomerular injury. (c) 2014 by John Wiley Sons, Inc.",
author = "Joshua Ooi and Gan, {Poh Yi} and Dragana Odobasic and Holdsworth, {Stephen Roger} and Kitching, {Arthur Richard}",
year = "2014",
doi = "10.1002/0471142735.im1527s107",
language = "English",
volume = "107",
pages = "1 -- 19",
journal = "Current Protocols in Immunology",
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TY - JOUR

T1 - T cell mediated autoimmune glomerular disease in mice

AU - Ooi, Joshua

AU - Gan, Poh Yi

AU - Odobasic, Dragana

AU - Holdsworth, Stephen Roger

AU - Kitching, Arthur Richard

PY - 2014

Y1 - 2014

N2 - Many forms of glomerulonephritis are mediated by autoimmunity. While autoantibodies are often pathogenic, cell-mediated immunity plays an important role in a number of forms of rapidly progressive glomerulonephritis. This unit describes the induction of cell-mediated autoimmune glomerular disease in mice. One disease model, experimental anti-glomerular basement membrane (GBM) disease, features autoreactivity to a well-defined component of type IV collagen found in the GBM, alpha3(IV)NC1. The other models the cell-mediated effector response in forms of renal vasculitis, where autoantibodies to myeloperoxidase result in systemic neutrophil activation, resulting in their localization to the glomerulus and the subsequent deposition of myeloperoxidase within glomerular capillaries. There, myeloperoxidase acts as a planted autoantigen and is recognized by effector autoreactive myeloperoxidase-specific T cells. These models are useful both in defining mechanisms germane to the development of autoimmunity to alpha3(IV)NC1 and myeloperoxidase, and in dissecting the role of cell-mediated responses in effecting glomerular injury. (c) 2014 by John Wiley Sons, Inc.

AB - Many forms of glomerulonephritis are mediated by autoimmunity. While autoantibodies are often pathogenic, cell-mediated immunity plays an important role in a number of forms of rapidly progressive glomerulonephritis. This unit describes the induction of cell-mediated autoimmune glomerular disease in mice. One disease model, experimental anti-glomerular basement membrane (GBM) disease, features autoreactivity to a well-defined component of type IV collagen found in the GBM, alpha3(IV)NC1. The other models the cell-mediated effector response in forms of renal vasculitis, where autoantibodies to myeloperoxidase result in systemic neutrophil activation, resulting in their localization to the glomerulus and the subsequent deposition of myeloperoxidase within glomerular capillaries. There, myeloperoxidase acts as a planted autoantigen and is recognized by effector autoreactive myeloperoxidase-specific T cells. These models are useful both in defining mechanisms germane to the development of autoimmunity to alpha3(IV)NC1 and myeloperoxidase, and in dissecting the role of cell-mediated responses in effecting glomerular injury. (c) 2014 by John Wiley Sons, Inc.

UR - http://onlinelibrary.wiley.com/doi/10.1002/0471142735.im1527s107/pdf

U2 - 10.1002/0471142735.im1527s107

DO - 10.1002/0471142735.im1527s107

M3 - Article

VL - 107

SP - 1

EP - 19

JO - Current Protocols in Immunology

JF - Current Protocols in Immunology

SN - 1934-3671

ER -