Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-12-30
pubmed:abstractText
Adhesion molecules expressed on surface membranes of lymphocytes and other leukocytes enable their entry into the lymphoid and other tissues. However, little is known about molecules that govern the transit of leukocytes through the parenchyma of lymphoid organs proper. We show that in comparison to blood leukocytes, the corresponding cells isolated from lymphoid organs, i.e., lymph nodes and spleen, have a significantly augmented expression of certain surface molecules. The helper and cytotoxic subsets of T cells, as well as B cells, display the increased expression of CD44, ICAM-1 and LFA-1, whereas B cells additionally show the augmented expression of MHC class II. In comparison with blood monocytes, splenic monocytes show the increased expression of ICAM-1 and MHC class II molecules. When compared with blood NK cells, splenic NK cells only show the increased expression of ICAM-1. The molecules, which we show to be up regulated upon the entry of leukocytes into lymphoid organs, could be involved in their retention within the tissue via cell-cell or cell-extracellular matrix interactions and in control of their transit through lymphoid tissues.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0882-0139
pubmed:author
pubmed:issnType
Print
pubmed:volume
33
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
439-52
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2004
pubmed:articleTitle
Blood lymphocytes, monocytes and NK cells modulate their expression of CD44, ICAM-1, LFA-1 and MHC class II after arrival into lymphoid organs.
pubmed:affiliation
Faculty of Medicine, Institute of Histology and Embryology, University of Belgrade, Visegradska 26, Belgrade YU-11000, Serbia and Montenegro. emilicen@etf.bg.ac.yu
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't