Linked Life Data

9790067

Source:http://linkedlifedata.com/resource/pubmed/id/9790067

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
1998-12-31
pubmed:abstractText
Previously, we have shown that myelin basic protein (MBP)-specific Lewis rat GP2.E5/R1 (R1) T cells cultured with antigen and irradiated syngeneic splenocytes (IrrSPL) in the presence of anti-CD4 and LRTC1 monoclonal antibodies (MAbs) become highly effective antigen presenting cells (APC). The purpose of these studies was to identify the ligand for the LRTC1 MAb and to determine whether this MAb affected MBP-stimulated IL-2 production and expression of MHC class II molecules by T cells. In the current studies, we show that the LRTC1 MAb specifically immunoprecipitated molecular species of approximately 95, 150, and 180 kD. Commercially available anti-CD18 (beta2 integrin, beta-chain of LFA-1, MAC-1, and p150, 95) and LRTC1 MAb immunoprecipitated proteins with identical mobilities on 1-D and 2-D SDS-PAGE gels. Moreover, anti-CD18 and LRTC1 immunoprecipitates also showed identical mobilities on 1-D gels after enzymatic cleavage of N-linked oligosaccharides and thereby had the same patterns of differential glycosylation. Anti-CD4 MAb W3/25 and LRTC1 MAb synergistically inhibited T-cell IL-2 mRNA and IL-2 bioactivity, but augmented antigen-stimulated surface I-A on R1 T cells. In conclusion, these studies describe the characteristics of a novel anti-LFA-1 MAb, LRTC1, which should prove useful in studying costimulatory and adhesion pathways among rat leukocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0272-457X
pubmed:author
pubmed:issnType
Print
pubmed:volume
17
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
331-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
A novel monoclonal antibody against rat LFA-1: blockade of LFA-1 and CD4 augments class II MHC expression on T cells.
pubmed:affiliation
Department of Microbiology and Immunology, East Carolina University School of Medicine, Greenville, NC 27858-4354, USA.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't