Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5969
pubmed:dateCreated
2010-2-26
pubmed:abstractText
CD4+ T cells are critical for host defense but are also major drivers of immune-mediated disease. These T cells specialize to become distinct subsets and produce restricted patterns of cytokines, which are tailored to combat various microbial pathogens. Although classically viewed as distinct lineages, recent work calls into question whether helper CD4+ T cell subsets are more appropriately viewed as terminally differentiated cells or works in progress. Herein, we review recent advances that pertain to this topic and the mechanisms that contribute to helper CD4+ T cell commitment and plasticity. The therapeutic implications of these new findings are also considered.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
1095-9203
pubmed:author
pubmed:issnType
Electronic
pubmed:day
26
pubmed:volume
327
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1098-102
pubmed:dateRevised
2011-3-1
pubmed:meshHeading
pubmed:year
2010
pubmed:articleTitle
Mechanisms underlying lineage commitment and plasticity of helper CD4+ T cells.
pubmed:affiliation
Molecular Immunology and Inflammation Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892-1616, USA. osheajo@mail.nih.gov
pubmed:publicationType
Journal Article, Review, Research Support, N.I.H., Intramural