Endogenous foxp3+ T-regulatory cells suppress anti-glomerular basement membrane nephritis View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2011-05

AUTHORS

Joshua D Ooi, Sarah L Snelgrove, Daniel R Engel, Katharina Hochheiser, Isis Ludwig-Portugall, Yuji Nozaki, Kim M O'Sullivan, Michael J Hickey, Stephen R Holdsworth, Christian Kurts, A Richard Kitching

ABSTRACT

Foxp3(+) T-regulatory cells (Tregs) may suppress pathogenic inflammation; however, although transferred Tregs lessen glomerulonephritis in mice, the role of endogenous foxp3(+) cells is not known. To study this, we characterized endogenous foxp3(+) cells in accelerated anti-glomerular basement membrane (GBM) nephritis by using foxp3(GFP) reporter mice to track their responses in early and established disease. Further, diphtheria toxin was used to ablate foxp3(+) Tregs in foxp3(DTR) mice after establishing an immune response. In this model, mice were immunized with sheep globulin in adjuvant, and sheep anti-mouse GBM globulin was injected after 4 days to initiate progressive histological and functional injury. Intrarenal leukocytic infiltrates were increased by day 3 but intrarenal foxp3(+) Tregs, present in interstitial and periglomerular areas, were only increased at day 7. Ablation of foxp3(+) Tregs after injection of anti-GBM globulin increased renal injury and systemic T-cell responses, including increased interferon-γ and interleukin-17A (IL-17A) production, but no change in antibody titers. Compared with foxp3(+) Tregs isolated from naive mice, those from immunized mice produced more IL-10 and more effectively regulated CD4(+)foxp3(-) responder T cells. Thus, endogenous foxp3(+) Tregs infiltrate the kidney in glomerulonephritis, and deleting foxp3(+) cells after the induction of immune responses upregulated T-cell reactions and enhanced disease. Hence, endogenous foxp3(+) cells have increased suppressive capacity after immune stimuli. More... »

PAGES

977-986

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ki.2010.541

DOI

http://dx.doi.org/10.1038/ki.2010.541

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1013260884

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/21248715


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