Linked Life Data

14686489

Source:http://linkedlifedata.com/resource/pubmed/id/14686489

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2003-12-22
pubmed:abstractText
B7-H1 was originally identified by homology analysis in comparison with B7-1 and B7-2, two molecules with important immunoregulatory functions. B7-H1, however, was broadly induced in the majority of peripheral tissues as well as hematopoietic cells. Upon binding to an as yet unidentified costimulatory receptor on primed T-cells, B7-H1 costimulates T-cell proliferation and preferentially induces interleukin 10 and interferon gamma. The costimulatory function of B7-H1 may be critical for enhancing maturation and differentiation of T-cells in lymphoid organs. Conversely, by binding to programmed death 1 receptors on activated T-cells and B-cells, B7-H1 may inhibit ongoing T-cell responses in peripheral tissues by inducing apoptosis and arresting cell-cycle progression. Although a positive regulatory role of B7-H1 has been demonstrated in vitro and in various animal models, a negative regulatory role of B7-H1 has also been documented in human diseases, including cancer, rheumatoid arthritis, and human immunodeficiency virus infection. Delineation of the complex interactions between B7-H1 and its receptors as well as its interplay with other ligands is critical for understanding this new immunoregulatory system. Precise manipulation of B7-H1 and its receptors may provide unique opportunities for designing new disease treatments.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Nov
pubmed:issn
0925-5710
pubmed:author
pubmed:issnType
Print
pubmed:volume
78
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
321-8
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed:year
2003
pubmed:articleTitle
Immunology of B7-H1 and its roles in human diseases.
pubmed:affiliation
Third Department of Internal Medicine, Nippon Medical School, Tokyo, Japan. tam@nms.ac.jp
pubmed:publicationType
Journal Article, Review