Linked Life Data

16568261

Source:http://linkedlifedata.com/resource/pubmed/id/16568261

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2006-4-26
pubmed:abstractText
The NKG2D receptor costimulates effector/memory CD8 T cells and is normally absent on CD4 T cells but can be induced by T cell antigen receptor complex stimulation and interleukin-15 (IL-15). Among its ligands are the human major histocompatibility complex class I-related MICA and MICB, which have a restricted tissue distribution but are frequently associated with malignancies and some microbial infections. Moreover, aberrant expression of MIC may promote autoimmune disease progression. Human T cell lymphotropic virus type I (HTLV-1)-associated myelopathy/tropical spastic paraparesis (HAM/TSP) is a chronic inflammatory disease of the central nervous system that resembles multiple sclerosis. Disease progression involves production of IL-15 and its receptor through transactivation by the viral Tax regulator protein, an activated immune response state, and local cytokine production and T cell fratricide by Tax-specific cytotoxic T lymphocytes (CTL). This study shows that as with CD8 T cells, substantial proportions of HAM/TSP patient CD4 T cells are positive for NKG2D and that large numbers of T cells from both subsets express MIC, which can be transactivated by Tax independent of nuclear factor kappaB. Engagement of MIC by NKG2D promotes spontaneous HAM/TSP T cell proliferation and, apparently, CTL activities against HTLV-1-infected T cells. These results reveal a viral strategy that may exploit immune stimulatory mechanisms to negotiate a balance between promotion and limitation of infected host T cell expansions.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0093-7711
pubmed:author
pubmed:issnType
Print
pubmed:volume
58
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
252-8
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:16568261-CD4-Positive T-Lymphocytes, pubmed-meshheading:16568261-CD8-Positive T-Lymphocytes, pubmed-meshheading:16568261-Case-Control Studies, pubmed-meshheading:16568261-Cell Proliferation, pubmed-meshheading:16568261-Cells, Cultured, pubmed-meshheading:16568261-Disease Progression, pubmed-meshheading:16568261-Histocompatibility Antigens Class I, pubmed-meshheading:16568261-Humans, pubmed-meshheading:16568261-Immunization, pubmed-meshheading:16568261-Intracellular Signaling Peptides and Proteins, pubmed-meshheading:16568261-NK Cell Lectin-Like Receptor Subfamily K, pubmed-meshheading:16568261-Neoplasm Proteins, pubmed-meshheading:16568261-Paraparesis, Tropical Spastic, pubmed-meshheading:16568261-Receptors, Immunologic, pubmed-meshheading:16568261-Receptors, Natural Killer Cell, pubmed-meshheading:16568261-Transcriptional Activation
pubmed:year
2006
pubmed:articleTitle
Immunostimulation by induced expression of NKG2D and its MIC ligands in HTLV-1-associated neurologic disease.
pubmed:affiliation
Clinical Research Division, Fred Hutchinson Cancer Research Center, 1100 Fairview Ave. N., Seattle, WA 98109, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural