Linked Life Data

18941119

Source:http://linkedlifedata.com/resource/pubmed/id/18941119

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2009-1-23
pubmed:abstractText
The adoptive transfer of regulatory Foxp3(+) T (Treg) cells has been shown in various animal models to prevent inflammatory immune and autoimmune diseases. Translation into therapeutic applications, however, is hindered by the lack of suitable techniques and markers. CD25, commonly used to isolate Treg cells from mice, has only limited value in humans as it is also present on proinflammatory CD4(+) effector cells. Here we show that clean populations of human Foxp3(+) Treg cells can be obtained with antibodies directed against CD49d. The marker is present on proinflammatory peripheral blood mononuclear cells but is absent on immune-suppressive Treg cells. Depletion with alpha-CD49d removes contaminating interferon-gamma (IFN-gamma)- and interleukin-17 (IL-17)-secreting cells from Treg preparations of CD4(+)CD25(high) cells. More importantly, in combination with alpha-CD127 it allows the isolation of "untouched" Foxp3(+) Treg (ie, cells that have not been targeted by an antibody during purification). The removal of CD49d(+)/CD127(+) cells leaves a population of Foxp3(+) Treg virtually free of contaminating CD25(+) effector cells. The cells can be expanded in vitro and are effective suppressors both in vitro and in vivo. Thus, CD49d provides access to highly pure populations of untouched Foxp3(+) Treg cells conferring maximal safety for future clinical applications.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
1528-0020
pubmed:author
pubmed:issnType
Electronic
pubmed:day
22
pubmed:volume
113
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
827-36
pubmed:meshHeading
pubmed:year
2009
pubmed:articleTitle
CD49d provides access to "untouched" human Foxp3+ Treg free of contaminating effector cells.
pubmed:affiliation
Max-Delbrück-Center for Molecular Medicine, Berlin, Germany.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't