Linked Life Data

20810991

Source:http://linkedlifedata.com/resource/pubmed/id/20810991

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2010-9-22
pubmed:abstractText
Allogeneic bone marrow transplantation is an effective treatment for a number of malignant and nonmalignant diseases (Applebaum. 2001. Nature. 411: 385-389 and Copelan. 2006. N Engl J Med. 354: 1813-1826). However, the application of this therapeutic modality has been impeded by a number of confounding side effects, the most frequent and severe of which is the development of graft-versus-host disease (GVHD) (Copelan. 2006. N Engl J Med. 354: 1813-1826 and Blazar and Murphy. 2005. Philos Trans R Soc Lond B Biol Sci. 360: 1747-1767). Alloreactive donor T cells are critical for causing GVHD (Fowler. 2006. Crit Rev Oncol Hematol. 57: 225-244 and Ferrara and Reddy. 2006. Semin Hematol. 43: 3-10), whereas recent data demonstrated a significant role for the naturally occurring thymic-derived donor CD4(+)CD25(+)Foxp3(+) regulatory T cells (Tregs) (Bluestone and Abbas. 2003. Nat Rev Immunol. 3: 253-257 and Shevach. 2006. Immunity. 25: 195-201) in suppressing experimental GVHD after bone marrow transplantation (Blazar and Taylor. 2005. Biol Blood Marrow Transpl. 11: 46-49 and Joffe and van Meerwijk. 2006. Semin Immunol. 18: 128-135) . Host APCs are required for induction of GVHD by the conventional donor T cells. However, it is not known whether they are also obligatory for donor Treg-mediated suppression of GVHD. Using multiple clinically relevant MHC-matched and -mismatched murine models of GVHD, we investigated the role of host APCs in the suppression of GVHD by donor Tregs. We found that alloantigen expression by the host APCs is necessary and sufficient for induction of GVHD protection by donor Tregs. This requirement was independent of their effect on the maintenance of Treg numbers and the production of IL-10 or IDO by the host APCs.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1550-6606
pubmed:author
pubmed:issnType
Electronic
pubmed:day
1
pubmed:volume
185
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
3866-72
pubmed:dateRevised
2011-4-27
pubmed:meshHeading
pubmed-meshheading:20810991-Animals, pubmed-meshheading:20810991-Antigen Presentation, pubmed-meshheading:20810991-Antigen-Presenting Cells, pubmed-meshheading:20810991-Bone Marrow Transplantation, pubmed-meshheading:20810991-Cell Separation, pubmed-meshheading:20810991-Disease Models, Animal, pubmed-meshheading:20810991-Flow Cytometry, pubmed-meshheading:20810991-Graft vs Host Disease, pubmed-meshheading:20810991-Histocompatibility Antigens Class II, pubmed-meshheading:20810991-Interleukin-2 Receptor alpha Subunit, pubmed-meshheading:20810991-Lymphocyte Activation, pubmed-meshheading:20810991-Mice, pubmed-meshheading:20810991-Mice, Inbred BALB C, pubmed-meshheading:20810991-Mice, Inbred C57BL, pubmed-meshheading:20810991-T-Lymphocyte Subsets, pubmed-meshheading:20810991-T-Lymphocytes, Regulatory
pubmed:year
2010
pubmed:articleTitle
A crucial role for host APCs in the induction of donor CD4+CD25+ regulatory T cell-mediated suppression of experimental graft-versus-host disease.
pubmed:affiliation
Department of Internal Medicine, University of Michigan Comprehensive Cancer Center, Ann Arbor, MI 48109, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural