Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2007-3-30
pubmed:abstractText
Forkhead box P3 (FOXP3) is currently thought to be the most specific marker for naturally occurring CD4(+)CD25(+) T regulatory cells (nTregs). In mice, expression of FoxP3 is strictly correlated with regulatory activity, whereas increasing evidence suggests that in humans, activated T effector cells (Teffs) may also express FOXP3. In order to better define the role of FOXP3 in human Teff cells, we investigated the intensity and kinetics of expression in ex vivo Teff cells, suppressed Teff cells and Teff cell lines. We found that all dividing Teff cells expressed FOXP3, but only transiently, and at levels that were significantly lower than those in suppressive nTregs. This temporary expression in Teff cells was insufficient to suppress expression of reported targets of FOXP3 repressor activity, including CD127, IL-2 and IFN-gamma, and was not correlated with induction of a nTreg phenotype. Thus expression of FOXP3 is a normal consequence of CD4(+) T cell activation and, in humans, it can no longer be used as an exclusive marker of nTregs. These data indicate that our current understanding of how FOXP3 contributes to immune tolerance in humans needs to be re-evaluated.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/2,3-bis(palmitoyloxy)-2-propyl-1-pal..., http://linkedlifedata.com/resource/pubmed/chemical/Antibodies, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD28, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD3, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation..., http://linkedlifedata.com/resource/pubmed/chemical/CD69 antigen, http://linkedlifedata.com/resource/pubmed/chemical/CTLA-4 Antigen, http://linkedlifedata.com/resource/pubmed/chemical/CTLA4 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Ctla4 protein, mouse, http://linkedlifedata.com/resource/pubmed/chemical/Cysteine, http://linkedlifedata.com/resource/pubmed/chemical/Cytokines, http://linkedlifedata.com/resource/pubmed/chemical/FOXP3 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Flagellin, http://linkedlifedata.com/resource/pubmed/chemical/Forkhead Transcription Factors, http://linkedlifedata.com/resource/pubmed/chemical/Glucocorticoid-Induced..., http://linkedlifedata.com/resource/pubmed/chemical/Interferon-gamma, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-2 Receptor alpha Subunit, http://linkedlifedata.com/resource/pubmed/chemical/Interleukin-7 Receptor alpha Subunit, http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type, http://linkedlifedata.com/resource/pubmed/chemical/Lipoproteins, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Nerve Growth Factor, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Tumor Necrosis Factor, http://linkedlifedata.com/resource/pubmed/chemical/TNFRSF18 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/Toll-Like Receptors
pubmed:status
MEDLINE
pubmed:month
Apr
pubmed:issn
0953-8178
pubmed:author
pubmed:issnType
Print
pubmed:volume
19
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
345-54
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:17329235-Antibodies, pubmed-meshheading:17329235-Antigens, CD, pubmed-meshheading:17329235-Antigens, CD28, pubmed-meshheading:17329235-Antigens, CD3, pubmed-meshheading:17329235-Antigens, Differentiation, pubmed-meshheading:17329235-Antigens, Differentiation, T-Lymphocyte, pubmed-meshheading:17329235-CD4-Positive T-Lymphocytes, pubmed-meshheading:17329235-CTLA-4 Antigen, pubmed-meshheading:17329235-Cell Line, pubmed-meshheading:17329235-Cell Proliferation, pubmed-meshheading:17329235-Clonal Anergy, pubmed-meshheading:17329235-Coculture Techniques, pubmed-meshheading:17329235-Cysteine, pubmed-meshheading:17329235-Cytokines, pubmed-meshheading:17329235-Flagellin, pubmed-meshheading:17329235-Forkhead Transcription Factors, pubmed-meshheading:17329235-Glucocorticoid-Induced TNFR-Related Protein, pubmed-meshheading:17329235-Humans, pubmed-meshheading:17329235-Interferon-gamma, pubmed-meshheading:17329235-Interleukin-2, pubmed-meshheading:17329235-Interleukin-2 Receptor alpha Subunit, pubmed-meshheading:17329235-Interleukin-7 Receptor alpha Subunit, pubmed-meshheading:17329235-Lectins, C-Type, pubmed-meshheading:17329235-Lipoproteins, pubmed-meshheading:17329235-Lymphocyte Activation, pubmed-meshheading:17329235-Receptors, Nerve Growth Factor, pubmed-meshheading:17329235-Receptors, Tumor Necrosis Factor, pubmed-meshheading:17329235-T-Lymphocyte Subsets, pubmed-meshheading:17329235-T-Lymphocytes, Regulatory, pubmed-meshheading:17329235-Toll-Like Receptors
pubmed:year
2007
pubmed:articleTitle
Activation-induced FOXP3 in human T effector cells does not suppress proliferation or cytokine production.
pubmed:affiliation
Department of Surgery, University of British Columbia, and Immunity and Infection Research Centre, Vancouver Coastal Health Research Institute, 2660 Oak Street, Vancouver, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't