Linked Life Data

16633862

Source:http://linkedlifedata.com/resource/pubmed/id/16633862

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
2006-8-15
pubmed:abstractText
The humanized monoclonal antibody (MAb) efalizumab (Raptiva) was developed to meet a longstanding need for specific, safe, and effective anti-psoriatic treatments. Efalizumab, which is directed at the lymphocyte surface protein LFA-1, prevents multiple interactions between T cells and other cell types. Here, we review the inflammatory pathway that drives the development of psoriasis, and we discuss several mechanisms by which efalizumab suppresses skin inflammation in psoriasis. Efalizumab reversibly increases circulating T-cell counts, as T cells--including pathogenic CD8 memory T cells that are prominent in psoriatic lesions-- are specifically restrained from leaving the bloodstream and entering the skin. Within two weeks of the onset of efalizumab treatment, cell surface and intracellular LFA-1 pools are substantially cleared by lysosomal degradation. Residual surface LFA-1 molecules remain saturated with bound efalizumab for some weeks following cessation of treatment. Efalizumab's pharmacodynamic properties are consistent with its profound and reversible beneficial effects on the histopathology of psoriatic skin.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1203-4754
pubmed:author
pubmed:issnType
Print
pubmed:volume
9 Suppl 1
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
4-9
pubmed:dateRevised
2007-7-4
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
Efalizumab, a reversible T-cell modulator for psoriasis.
pubmed:affiliation
Sunnybrook & Women's College Health Sciences Centre, University of Toronto Medical School and Ventana Clinical Research Corp., Toronto, ON. neil.shear@sw.ca
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't