Regulation by CD25+ lymphocytes of autoantigen-specific T-cell responses in Goodpasture's (anti-GBM) disease View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2003-11

AUTHORS

Alan D Salama, Afzal N Chaudhry, Kathryn A Holthaus, Karen Mosley, Raghu Kalluri, Mohamed H Sayegh, Robert I Lechler, Charles D Pusey, Liz Lightstone

ABSTRACT

BACKGROUND: Goodpasture's, or anti-glomerular basement membrane (GBM), disease is unusual among autoimmune diseases in that it rarely follows a relapsing-remitting course. Moreover, untreated, autoantibodies disappear spontaneously after 1 to 3 years and, following treatment, autoreactive T cells diminish in frequency. This suggests that operational tolerance toward the autoantigen is reestablished. However, the mechanisms underlying this have remained unclear. Recent data have suggested that a population of regulatory T lymphocytes can suppress both autoimmune and alloimmune responses in animal models and are present in normal individuals. However, to date, they have not been demonstrated to play a role in human renal autoimmune disease. METHODS: We studied the role of regulatory CD25+ cells in suppressing T-cell responses to the Goodpasture autoantigen in nine patients with Goodpasture's disease. RESULTS: At the time of acute presentation, there was no evidence of a regulatory cell population. However, from 3 months onward a population emerged, capable of suppressing the response to the Goodpasture autoantigen. Following depletion of CD25+ cells, the frequencies of autoreactive-, GBM-, or collagen alpha 3(IV)NC1-specific T cells were significantly increased (P = 0.031 by paired t test), with five of seven (71%) convalescent patients and no acute patients demonstrating regulation. CONCLUSION: These data demonstrate that, in Goodpasture's disease, regulatory CD25+ T cells play a role in inhibiting the autoimmune response. Their emergence and persistence may underlie the "single hit" nature of this condition. Understanding the conditions required for the development and propagation of these cells would allow development of novel therapeutic strategies for inducing hyporesponsiveness in autoimmune disease. More... »

PAGES

1685-1694

Identifiers

URI

http://scigraph.springernature.com/pub.10.1046/j.1523-1755.2003.00259.x

DOI

http://dx.doi.org/10.1046/j.1523-1755.2003.00259.x

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1004405762

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/14531801


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Download the RDF metadata as:  json-ld nt turtle xml License info

HOW TO GET THIS DATA PROGRAMMATICALLY:

JSON-LD is a popular format for linked data which is fully compatible with JSON.

curl -H 'Accept: application/ld+json' 'https://scigraph.springernature.com/pub.10.1046/j.1523-1755.2003.00259.x'

N-Triples is a line-based linked data format ideal for batch operations.

curl -H 'Accept: application/n-triples' 'https://scigraph.springernature.com/pub.10.1046/j.1523-1755.2003.00259.x'

Turtle is a human-readable linked data format.

curl -H 'Accept: text/turtle' 'https://scigraph.springernature.com/pub.10.1046/j.1523-1755.2003.00259.x'

RDF/XML is a standard XML format for linked data.

curl -H 'Accept: application/rdf+xml' 'https://scigraph.springernature.com/pub.10.1046/j.1523-1755.2003.00259.x'


 

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