rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
5
|
pubmed:dateCreated |
2003-2-20
|
pubmed:abstractText |
Murine CD4(+)CD25(+) regulatory cells have been reported to express latency-associated peptide (LAP) and TGF-beta on the surface after activation, and exert regulatory function by the membrane-bound TGF-beta in vitro. We have now found that a small population of CD4(+) T cells, both CD25(+) and CD25(-), can be stained with a goat anti-LAP polyclonal Ab without being stimulated. Virtually all these LAP(+) cells are also positive for thrombospondin, which has the ability to convert latent TGF-beta to the active form. In the CD4(+)CD45RB(high)-induced colitis model of SCID mice, regulatory activity was exhibited not only by CD25(+)LAP(+) and CD25(+)LAP(-) cells, but also by CD25(-)LAP(+) cells. CD4(+)CD25(-)LAP(+) T cells were part of the CD45RB(low) cell fraction. CD4(+)CD25(-)LAP(-)CD45RB(low) cells had minimal, if any, regulatory activity in the colitis model. The regulatory function of CD25(-)LAP(+) cells was abrogated in vivo by anti-TGF-beta mAb. These results identify a new TGF-beta-dependent regulatory CD4(+) T cell phenotype that is CD25(-) and LAP(+).
|
pubmed:grant |
|
pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
AIM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Mar
|
pubmed:issn |
0022-1767
|
pubmed:author |
|
pubmed:issnType |
Print
|
pubmed:day |
1
|
pubmed:volume |
170
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
2516-22
|
pubmed:dateRevised |
2007-11-15
|
pubmed:meshHeading |
pubmed-meshheading:12594277-Animals,
pubmed-meshheading:12594277-Antibodies,
pubmed-meshheading:12594277-Antigens, CD45,
pubmed-meshheading:12594277-Biotinylation,
pubmed-meshheading:12594277-CD4-Positive T-Lymphocytes,
pubmed-meshheading:12594277-Cell Membrane,
pubmed-meshheading:12594277-Cells, Cultured,
pubmed-meshheading:12594277-Coculture Techniques,
pubmed-meshheading:12594277-Colitis,
pubmed-meshheading:12594277-Cytokines,
pubmed-meshheading:12594277-Disease Models, Animal,
pubmed-meshheading:12594277-Female,
pubmed-meshheading:12594277-Flow Cytometry,
pubmed-meshheading:12594277-Goats,
pubmed-meshheading:12594277-Immunophenotyping,
pubmed-meshheading:12594277-Male,
pubmed-meshheading:12594277-Mice,
pubmed-meshheading:12594277-Mice, Inbred BALB C,
pubmed-meshheading:12594277-Mice, SCID,
pubmed-meshheading:12594277-Peptide Fragments,
pubmed-meshheading:12594277-Protein Precursors,
pubmed-meshheading:12594277-Receptors, Interleukin-2,
pubmed-meshheading:12594277-Staining and Labeling,
pubmed-meshheading:12594277-T-Lymphocyte Subsets,
pubmed-meshheading:12594277-Transforming Growth Factor beta,
pubmed-meshheading:12594277-Transforming Growth Factor beta1
|
pubmed:year |
2003
|
pubmed:articleTitle |
CD4+CD25- T cells that express latency-associated peptide on the surface suppress CD4+CD45RBhigh-induced colitis by a TGF-beta-dependent mechanism.
|
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
|