Linked Life Data

12207337

Source:http://linkedlifedata.com/resource/pubmed/id/12207337

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
9
pubmed:dateCreated
2002-9-3
pubmed:abstractText
CD44 has been implicated in hyaluronan (HA)-dependent primary adhesion between leukocytes and endothelium. We studied the trafficking of lymphocytes of CD44-deficient DBA/1 mice under normal conditions, and during chronic and transient forms of inflammation. Animals homozygous for the CD44 mutation (CD44(-/-)) showed no abnormalities in the composition of the lympho-hemopoietic system, but their leukocytes could not recognize HA as an adhesion ligand. T cells from CD44-deficient mice responded normally to immunization with type II collagen or stimulation with a bacterial superantigen. Lymphocytes harvested from naive CD44(-/-) and wild-type (WT) animals showed similar trafficking properties when injected into naive recipients. However, cells from WT and CD44-deficient mice with collagen-induced arthritis showed distinct migration kinetics upon transfer to arthritic recipients. While lymphocytes from CD44(-/-) mice preferentially homed to lymph nodes, their entry into the inflamed synovial joints was delayed as compared with WT cells. Similar differences were observed in the migration kinetics of CD44-deficient and CD44-competent (CD44(+/+)) lymphocytes in bacterial superantigen-induced peritonitis. These results suggest that CD44 plays opposite roles in the regulation of leukocyte traffic to inflammatory sites versus the lymph nodes. CD44-deficient lymphocytes from animals with chronic arthritis, but not from those with transient peritonitis, expressed markedly reduced levels of the lymph node homing receptor, L-selectin. Extreme down-modulation of L-selectin from CD44(-/-) cells in arthritic condition might be a counter-regulatory response, which, by extending lymphocyte transit time in the circulation at the expense of lymph node homing, allows CD44-deficient cells to gain entry to the site of chronic inflammation via secondary adhesion mechanisms.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0014-2980
pubmed:author
pubmed:issnType
Print
pubmed:volume
32
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
2532-42
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:12207337-Animals, pubmed-meshheading:12207337-Antigens, CD44, pubmed-meshheading:12207337-Arthritis, Experimental, pubmed-meshheading:12207337-Cell Adhesion, pubmed-meshheading:12207337-Chemotaxis, Leukocyte, pubmed-meshheading:12207337-Chronic Disease, pubmed-meshheading:12207337-Collagen Type II, pubmed-meshheading:12207337-Enterotoxins, pubmed-meshheading:12207337-Hyaluronic Acid, pubmed-meshheading:12207337-L-Selectin, pubmed-meshheading:12207337-Lymphocyte Transfusion, pubmed-meshheading:12207337-Male, pubmed-meshheading:12207337-Mice, pubmed-meshheading:12207337-Mice, Inbred DBA, pubmed-meshheading:12207337-Mice, Knockout, pubmed-meshheading:12207337-Peritonitis, pubmed-meshheading:12207337-Receptors, Antigen, T-Cell, alpha-beta, pubmed-meshheading:12207337-Receptors, Lymphocyte Homing, pubmed-meshheading:12207337-Superantigens
pubmed:year
2002
pubmed:articleTitle
Trafficking of CD44-deficient murine lymphocytes under normal and inflammatory conditions.
pubmed:affiliation
Section of Biochemistry and Molecular Biology, Department of Orthopedic Surgery, Rush University at Rush-Presbyterian-St. Luke's Medical Center, Chicago 60612, USA.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, U.S. Gov't, P.H.S.