Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1990-7-20
pubmed:abstractText
Lymphocyte migration into the lymphoid organs and sites of inflammation is controlled by lymphocyte-endothelial cell interaction at sites where lymphocytes exit from the blood. Expression of Hermes-defined CD44 class of lymphocyte homing receptor and HECA-452 antigen specific for high-endothelium-mediating physiologic lymphocyte extravasation was studied in dermatitis herpetiformis, celiac disease, psoriasis, mycosis fungoides, lymphocytosis cutis, atopic dermatitis, and allergic contact dermatitis. Also, duodenal biopsies of patients suffering from dermatitis herpetiformis or celiac disease were studied for existence of these antigens. Infiltrating lymphocytes in the skin and in the duodenal area expressed homing receptor molecules when studied with monoclonal antibodies, Hermes-1 and Hermes-3, that recognize the CD44 class of molecules involved in lymphocyte binding to high endothelial venules in peripheral lymph nodes, mucosa-associated lymphatic tissues, and inflamed synovium. However, the HECA-452 antigen was not detected on the venules, neither in the skin nor in the duodenum. Even the venules possessing high endothelium morphologically were HECA-452 negative. These findings suggest the CD44 class of lymphocyte homing receptor(s) is also involved in lymphocyte homing to inflamed skin and the duodenal area of the gut. However, on the basis of HECA-452 staining, high endothelial venules in inflamed skin and duodenum are not antigenically identical with high endothelial venules in organized lymphoid tissues. This finding indirectly supports the idea that molecules and/or mechanisms mediating lymphocyte extravasation might be distinct in these organs.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0022-202X
pubmed:author
pubmed:issnType
Print
pubmed:volume
94
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
786-92
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:1693939-Adult, pubmed-meshheading:1693939-Aged, pubmed-meshheading:1693939-Antibodies, pubmed-meshheading:1693939-Antibodies, Monoclonal, pubmed-meshheading:1693939-Antigens, CD, pubmed-meshheading:1693939-Antigens, Differentiation, pubmed-meshheading:1693939-Cell Adhesion Molecules, pubmed-meshheading:1693939-Cell Movement, pubmed-meshheading:1693939-Endothelium, pubmed-meshheading:1693939-Endothelium, Lymphatic, pubmed-meshheading:1693939-Factor VIII, pubmed-meshheading:1693939-Female, pubmed-meshheading:1693939-Humans, pubmed-meshheading:1693939-Intercellular Adhesion Molecule-1, pubmed-meshheading:1693939-Lymphocytes, pubmed-meshheading:1693939-Male, pubmed-meshheading:1693939-Middle Aged, pubmed-meshheading:1693939-Receptors, Lymphocyte Homing, pubmed-meshheading:1693939-Skin, pubmed-meshheading:1693939-Staining and Labeling
pubmed:year
1990
pubmed:articleTitle
Lymphocyte migration into the skin: the role of lymphocyte homing receptor (CD44) and endothelial cell antigen (HECA-452).
pubmed:affiliation
Department of Medical Microbiology, Turku University, Finland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't