Linked Life Data

17641028

Source:http://linkedlifedata.com/resource/pubmed/id/17641028

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2007-7-20
pubmed:abstractText
T cell activation is associated with a dramatic reorganization of cell surface proteins and associated signaling components into discrete subdomains within the immunological synapse in T cell:APC conjugates. However, the signals that direct the localization of these proteins and the functional significance of this organization have not been established. In this study, we have used wild-type and LFA-1-deficient, DO11.10 TCR transgenic T cells to examine the role of LFA-1 in the formation of the immunological synapse. We found that coengagement of LFA-1 is not required for the formation of the central supramolecular activation cluster (cSMAC) region, but does increase the accumulation of TCR/class II complexes within the cSMAC. In addition, LFA-1 is required for the recruitment and localization of talin into the peripheral supramolecular activation cluster region and exclusion of CD45 from the synapse. The ability of LFA-1 to increase the amount of TCR engaged during synapse formation and segregate the phosphatase, CD45, from the synapse suggests that LFA-1 might enhance proximal TCR signaling. To test this, we combined flow cytometry-based cell adhesion and calcium-signaling assays and found that coengagement of LFA-1 significantly increased the magnitude of the intracellular calcium response following Ag presentation. These data support the idea that in addition to its important role on regulating T cell:APC adhesion, coengagement of LFA-1 can enhance T cell signaling, and suggest that this may be accomplished in part through the organization of proteins within the immunological synapse.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
179
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1616-24
pubmed:dateRevised
2011-11-7
pubmed:meshHeading
pubmed-meshheading:17641028-Adjuvants, Immunologic, pubmed-meshheading:17641028-Animals, pubmed-meshheading:17641028-Antigen-Presenting Cells, pubmed-meshheading:17641028-Antigens, CD45, pubmed-meshheading:17641028-Cell Communication, pubmed-meshheading:17641028-Cell Line, Tumor, pubmed-meshheading:17641028-Histocompatibility Antigens Class II, pubmed-meshheading:17641028-Lymphocyte Activation, pubmed-meshheading:17641028-Lymphocyte Function-Associated Antigen-1, pubmed-meshheading:17641028-Mice, pubmed-meshheading:17641028-Mice, Inbred BALB C, pubmed-meshheading:17641028-Mice, Knockout, pubmed-meshheading:17641028-Mice, Transgenic, pubmed-meshheading:17641028-Receptors, Antigen, T-Cell, pubmed-meshheading:17641028-Signal Transduction, pubmed-meshheading:17641028-T-Lymphocytes, pubmed-meshheading:17641028-Talin, pubmed-meshheading:17641028-Up-Regulation
pubmed:year
2007
pubmed:articleTitle
LFA-1-mediated T cell costimulation through increased localization of TCR/class II complexes to the central supramolecular activation cluster and exclusion of CD45 from the immunological synapse.
pubmed:affiliation
David H. Smith Center for Vaccine Biology and Immunology, University of Rochester, NY 14642, USA.
pubmed:publicationType
Journal Article, Research Support, N.I.H., Extramural