Source:http://linkedlifedata.com/resource/pubmed/id/17589510
Switch to
| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
8
|
| pubmed:dateCreated |
2007-7-20
|
| pubmed:abstractText |
Regulated glycosylation controls T cell processes, including activation, differentiation and homing by creating or masking ligands for endogenous lectins. Here we show that stimuli promoting T helper type 1 (TH1), TH2 or interleukin 17-producing T helper (TH-17) differentiation can differentially regulate the glycosylation pattern of T helper cells and modulate their susceptibility to galectin-1, a glycan-binding protein with anti-inflammatory activity. Although TH1- and TH-17-differentiated cells expressed the repertoire of cell surface glycans critical for galectin-1-induced cell death, TH2 cells were protected from galectin-1 through differential sialylation of cell surface glycoproteins. Consistent with those findings, galectin-1-deficient mice developed greater TH1 and TH-17 responses and enhanced susceptibility to autoimmune neuroinflammation. Our findings identify a molecular link among differential glycosylation of T helper cells, susceptibility to cell death and termination of the inflammatory response.
|
| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
|
| pubmed:issn |
1529-2908
|
| pubmed:author |
pubmed-author:BaumLinda GLG,
pubmed-author:BiancoGermán AGA,
pubmed-author:CorrealeJorgeJ,
pubmed-author:CrociDiego ODO,
pubmed-author:HernandezJoseph DJD,
pubmed-author:IlarreguiJuan MJM,
pubmed-author:PoirierFrancoiseF,
pubmed-author:RabinovichGabriel AGA,
pubmed-author:RileyEleanor MEM,
pubmed-author:ToscanoMarta AMA,
pubmed-author:ZwirnerNorberto WNW
|
| pubmed:issnType |
Print
|
| pubmed:volume |
8
|
| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
|
| pubmed:pagination |
825-34
|
| pubmed:dateRevised |
2007-11-8
|
| pubmed:meshHeading |
pubmed-meshheading:17589510-Adoptive Transfer,
pubmed-meshheading:17589510-Animals,
pubmed-meshheading:17589510-Apoptosis,
pubmed-meshheading:17589510-Cell Differentiation,
pubmed-meshheading:17589510-Encephalomyelitis, Autoimmune, Experimental,
pubmed-meshheading:17589510-Flow Cytometry,
pubmed-meshheading:17589510-Galectin 1,
pubmed-meshheading:17589510-Glycosylation,
pubmed-meshheading:17589510-Humans,
pubmed-meshheading:17589510-Immunoblotting,
pubmed-meshheading:17589510-In Situ Nick-End Labeling,
pubmed-meshheading:17589510-Inflammation,
pubmed-meshheading:17589510-Interleukin-17,
pubmed-meshheading:17589510-Membrane Glycoproteins,
pubmed-meshheading:17589510-Mice,
pubmed-meshheading:17589510-Polysaccharides,
pubmed-meshheading:17589510-T-Lymphocyte Subsets,
pubmed-meshheading:17589510-T-Lymphocytes, Helper-Inducer,
pubmed-meshheading:17589510-Th1 Cells,
pubmed-meshheading:17589510-Th2 Cells
|
| pubmed:year |
2007
|
| pubmed:articleTitle |
Differential glycosylation of TH1, TH2 and TH-17 effector cells selectively regulates susceptibility to cell death.
|
| pubmed:affiliation |
División de Immunogenética. Hospital de Clínicas José de San Martín, Facultad de Medicina, Universidad de Buenos Aires, C1120AAF Buenos Aires, Argentina.
|
| pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
|