Linked Life Data

8977279

Source:http://linkedlifedata.com/resource/pubmed/id/8977279

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
12
pubmed:dateCreated
1997-2-4
pubmed:abstractText
To assess the capacity of major histocompatibility complex (MHC) class II-binding competitor peptides in inhibiting antibody-mediated disease processes, we studied experimental autoimmune myasthenia gravis in Lewis rats. Experimental autoimmune myasthenia gravis, a disease model mediated by T cell-dependent autoantibodies against acetylcholine receptors, was induced by immunization with Torpedo californica acetylcholine receptor emulsified in complete Freund's adjuvant. The immunodominant acetylcholine receptor T cell epitope was recognized by T cells in the context of MHC class II RT1.B(L). The disease inhibitory capacity of RT1.B(L)-binding peptides not related to the acetylcholine receptor was determined upon co-immunization with Torpedo acetylcholine receptor. Co-immunization of peptide OVA323-339, a strong RT1.B(L)-binding competitor peptide, resulted in complete disease inhibition. Although, the priming of the anti-acetylcholine receptor T cell response was not fully inhibited, the kinetics of the response was changed. Moreover, besides a drastic reduction of the anti-Torpedo acetylcholine receptor antibody titers, a shift in isotype distribution was found. These findings indicate that antibody-mediated autoimmune processes can be suppressed by MHC class II competitor peptides. Furthermore, the administration of such peptides in vivo not only passively inhibits T cell activation, but also functionally alters the immune response.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0014-2980
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2866-75
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1996
pubmed:articleTitle
Inhibition of experimental autoimmune myasthenia gravis by major histocompatibility complex class II competitor peptides results not only in a suppressed but also in an altered immune response.
pubmed:affiliation
Institute of Infectious Diseases and Immunology, Faculty of Veterinary Medicine, Utrecht University, The Netherlands. M.Wauben@vetmic.dgk.ruu.nl
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't