Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
43
pubmed:dateCreated
2004-10-27
pubmed:abstractText
SJL mice are highly susceptible to experimental autoimmune encephalomyelitis (EAE) induced with myelin proteolipid protein (PLP) peptide 139-151, whereas H-2 congenic B10.S mice are resistant. Immunodominance and susceptibility to EAE are associated with a high precursor frequency of PLP 139-151-specific T cells in the naive repertoire of SJL mice. To understand the mechanism of EAE resistance in B10.S mice, we determined the precursor frequency of PLP 139-151-reactive T cells in both strains by using IAs/PLP 139-151 tetramers. SJL and B10.S mice had similar frequencies of tetramer-reactive T cells in the naive peripheral repertoire. However, in SJL mice, the majority of PLP 139-151 tetramer-positive cells were in the CD4+CD25- population, whereas there were more tetramer-positive cells in the CD4+CD25+ population of B10.S mice. Depletion of CD4+CD25+ cells in vivo facilitated the expansion of PLP 139-151-reactive cells with production of T helper 1 cytokines in EAE-resistant B10.S mice. Furthermore, anti-CD25 Ab treatment before immunization resulted in EAE induction in these otherwise resistant mice. These data indicate an important role for autoantigen-specific CD4+CD25+ cells in genetic resistance to autoimmunity.
pubmed:grant
pubmed:commentsCorrections
http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-10075980, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-10464178, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-10605010, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-10704458, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-10850488, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-11276194, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-11276200, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-11390442, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-11514600, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-12517952, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-12522256, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-12612581, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-12975475, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-14530340, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-2465343, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-6371137, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-6806429, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-7584131, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-7636184, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-8598487, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-8757345, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-8786337, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-9670041, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-9712054, http://linkedlifedata.com/resource/pubmed/commentcorrection/15492218-9988264
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0027-8424
pubmed:author
pubmed:issnType
Print
pubmed:day
26
pubmed:volume
101
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
15434-9
pubmed:dateRevised
2009-11-18
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Myelin proteolipid protein-specific CD4+CD25+ regulatory cells mediate genetic resistance to experimental autoimmune encephalomyelitis.
pubmed:affiliation
Center for Neurologic Diseases, Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't