title: Expression of ICAM-R (ICAM-3), a novel counter-receptor for LFA-1, in rheumatoid and nonrheumatoid synovium. Comparison with other adhesion molecules.
abstract: OBJECTIVE
  To study the distribution of intercellular adhesion molecule receptor (ICAM-R, or ICAM-3), a novel ligand for the leukointegrin lymphocyte function-associated antigen 1 (LFA-1), in normal and rheumatoid synovial membranes and to compare this with the distribution of ICAM-1, ICAM-2, vascular cell adhesion molecule 1 (VCAM-1), and endothelial leukocyte adhesion molecule 1 (ELAM-1).
  
  
  METHODS
  We performed immunohistochemical analyses of frozen sections of normal and rheumatoid synovial tissue using monoclonal antibodies to the molecules examined.
  
  
  RESULTS
  ICAM-1 staining was detectable on the vascular endothelium and the synovial lining cells of both normal and rheumatoid synovial membranes. A variable proportion of lymphocytes infiltrating rheumatoid tissues expressed ICAM-1, ICAM-2 staining was demonstrable in the vascular endothelium of both normal and inflamed tissues, the latter demonstrating a significantly higher proportion of positive vessels. ELAM-1 staining was not detectable in normal synovial membranes but was seen on the endothelium of a limited number of rheumatoid synovial vessels, usually close to the synovial lining cell layer. VCAM-1 staining was intense in both normal and rheumatoid synovial lining cells, but vascular staining was weak in both. In contrast, ICAM-R staining was not detected in association with any synovial blood vessels, but was widely expressed by lymphocytes and macrophages. Cells of the lining layer did not stain for ICAM-R.
  
  
  CONCLUSIONS
  Although ICAM-R is a ligand for LFA-1 and shares considerable sequence homology with ICAM-1 and ICAM-2, it does not appear to be expressed by the endothelium of normal or inflamed synovial vessels. Intense expression of ICAM-R by rheumatoid synovial lymphocytes and macrophages suggests that it may play a role in processes requiring cell-cell contact, such as antigen presentation and homotypic aggregation.
authors.affiliation: Rheumatic Disease Unit, Winnipeg, Manitoba, Canada.
authors.forename: H
authors.initials: H
authors.lastname: el-Gabalawy
authors.forename: M
authors.initials: M
authors.lastname: Gallatin
authors.forename: R
authors.initials: R
authors.lastname: Vazeux
authors.forename: G
authors.initials: G
authors.lastname: Peterman
authors.forename: J
authors.initials: J
authors.lastname: Wilkins
mesh_terms: D015703:Antigens, CD; D001172:Arthritis, Rheumatoid / Q000473:pathology; D015815:Cell Adhesion Molecules / Q000032:analysis*; D019040:E-Selectin; D004730:Endothelium, Vascular / Q000737:chemistry; D006801:Humans; D018799:Intercellular Adhesion Molecule-1; D008214:Lymphocytes / Q000737:chemistry; D013583:Synovial Membrane / Q000737:chemistry* / Q000473:pathology; D019010:Vascular Cell Adhesion Molecule-1
chemical_list: D015703:Antigens, CD; D015815:Cell Adhesion Molecules; D019040:E-Selectin; C065289:ICAM2 protein, human; D019010:Vascular Cell Adhesion Molecule-1; D018799:Intercellular Adhesion Molecule-1