Immunohistologic analysis of the distribution of cell adhesion molecules within the inflammatory synovial microenvironment

Hale, Laura P.; Martin, Margaret E.; McCollum, Donald E.; Nunley, James A.; Springer, Timothy A.; Singer, Kay H.; Haynes, Barton F.

doi:10.1002/anr.1780320105

Cited by 181 publications

(78 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…33, No. 12 (December 1990) been localized in RA synovial tissues and in osteoarthritis synovial tissues by immunocytochemical techniques (8). Our studies extend these initial observations.…”

supporting

confidence: 77%

“…It has been demonstrated that the RA synovium contains cells that express HLA-DR antigens (4-7). There is also evidence that indicates that cells populating the inflamed tissue lining the RA joint have adhesion molecules as ligands for homing receptors on circulating T lymphocytes (8,9). It is hypothesized that the increased adhesiveness of the inflamed synovial tissue may play a central role in lymphocyte homing and retention in the diseased joint.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Role of cytokines in inflammatory synovitis

Chin

Winterrowd

Krzesicki

et al. 1990

Arthritis & Rheumatism

118

View full text Add to dashboard Cite

This study was undertaken in an effort to understand the role of cytokines in T lymphocyte trafficking into inflamed synovium and in the potential enhancement of antigen presentation by human synovial fibroblasts. We found that interleukin-lp (IL-lp), tumor necrosis factor a (TNFa), and interferon-y (IFNy) each increased the cell surface expression of intercellular adhesion molecule I (ICAM-I) on human synovial fibroblasts in a dose-and time-dependent manner. Maximal ICAM-1 expression occurred within 8 hours of induction, with the following order of efficacy: IFNy > TNFa > IL-1p. The number of cells bearing the ICAM-1 antigen also increased, from a basal level of -30% to more than 83% after cytokine induction (for all 3 cytokines). ICAM-1 expression rapidly decreased fdlowing cytokine removal. The expression of lymphocyte function-associated antigen 3 was also examined, but it was not changed by any of the 3 cytokines. Class I major histocompatibility complex antigen expression was increased modestly by all 3 cytokines, and expression was maximal by 24 hours after treatment. Only IFNy induced HLA class I1 antigen expression, and this expression persisted for up to 6 days following removal of the lymphokine. IL-6 and granulocyte-macrophage colony- stimulating factor had no effect on any of the parameters examined. Our data support an interactive role for inflammatory cytokines and the expression of adhesion ligands and HLA antigens by human synovial fibroblasts in the pathogenesis of synovial inflammation in rheumatoid arthritis.Rheumatoid arthritis (RA) is a chronic inflammatory autoimmune disease characterized in part by the proliferation of pannus tissue in diseased joints, which leads to eventual degradation of the articular cartilage and the subchondral bone (1)(2)(3). It has been demonstrated that the RA synovium contains cells that express HLA-DR antigens (4-7). There is also evidence that indicates that cells populating the inflamed tissue lining the RA joint have adhesion molecules as ligands for homing receptors on circulating T lymphocytes (8,9). It is hypothesized that the increased adhesiveness of the inflamed synovial tissue may play a central role in lymphocyte homing and retention in the diseased joint. The current study was initiated in an effort to elucidate cellular mechanisms that may be involved in chronic inflammatory synovitis. We examined the time and dose effects of various cytokines present in the inflammatory microenvironment in RA (10) on the expression of adhesion ligands intercellular adhesion molecule I (ICAM-1) and lymphocyte function-associated antigen 3 (LFA-3), and the expression of class I and class I1 major histocompatibility complex (MHC) antigens, 4 fibroblast cell surface molecules whose regulation may play critical roles in synovial inflammation.In previous studies, interferon-y (IFNy) has been shown to induce the expression of class I1 MHC antigens on synovial fibroblasts (1 l), and ICAM-1 has MATERIALS AND METHODSRecombinant cytokines and antibodies. Recombinant human i...

show abstract

supporting

confidence: 77%

mentioning

confidence: 99%

Role of cytokines in inflammatory synovitis

Chin

Winterrowd

Krzesicki

et al. 1990

Arthritis & Rheumatism

118

View full text Add to dashboard Cite

show abstract

“…However, the possibility that these cells are of synovial origin cannot be excluded as cells of the monocyte/macrophage lineage are found within or lining synovial tissue (Edwards, 1982;Athanasou et al, 1988). Synovial lining cells have an antigen phenotype which closely resembles that of tissue macrophages being characterised by weak or low frequency expression of CD Ila and also CDlIc (Hale et al, 1989;Allen et al, 1989), features not noted in the cases studied.…”

Section: Discussionmentioning

confidence: 79%

Bone resorption by macrophage polykaryons of giant cell tumour of tendon sheath

Athanasou

Quinn²,

Ferguson³

et al. 1991

Br J Cancer

View full text Add to dashboard Cite

Summary The antigenic phenotype, ultrastructure and bone resorbing ability of mononuclear and multinucleated giant cells of four giant cell tumour of tendon sheath (GCTTS) lesions was assessed. Both the giant cells and the mononuclear cells exhibted the antigenic phenotype of cells of the monocyte/macrophage lineage. The giant cells, unlike osteoclasts, did not respond morphologically to calcitonin and showed ultrastructural and immunophenotypic features of macrophage polykaryons. However (Wood et al., 1988), and do not support the concept that the lesion is a form of xanthoma or benign fibrous histiocytoma (Rosai, 1981).There have been several recent studies on the nature of giant cells in giant cell lesions of bone and soft tissue which have used bone resorption as an operational or functional criterion to determine whether tumour-associated giant cells present in a pathological lesion are osteoclasts (Athanasou et al., 1983;Flanagan & Chambers, 1988;Flanagan & Chambers, 1989 Materials and methodsBovine parathyroid hormone (PTH) (2,500 U mg ')was provided by Dr J. Zanelli (National Institute for Biological Standards, London, UK) and dissolved (230 IU ml-') in 1 ml 0.001 % acetic acid in distilled water containing 1 mg ml1' of bovine serum albumin (Sigma, UK) (BSA). Salmon calcitonin (CT) was donated by Armour Pharmaceuticals, Eastbourne, UK (4,450 IU mg-1) and dissolved (1 mg ml') in 0.05% NaCl and 0.2% sodium acetate in distilled water containing 1 mg ml-' of BSA. Prostaglandin E2 (Sigma) (PGE2) was dissolved (10-2 M) in alcohol. 1,25-Dihydroxy vitamin D3 [1, was donated by Roche products (Welwyn Garden City, UK) and dissolved (10-2 M) in alcohol. Interleukin-1 (IL-1) was kindly provided by Dr J. Saklatvala and dissolved (200 ng ml-') in RPMI.Four GCTTS lesions were examined. These were from the left index finger of a 37 year old female, the right index finger of a 58 year old male and the right and left middle fingers of a 45 year old male. In all cases, part of the lesion was fixed in formalin and processed routinely. For transmission electron microscopy, tiny samples of tissue were fixed in 4%phosphate buffered glutaraldehyde for 6 h, then post-fixed_in 2% buffered osmium tetroxide for 2 h. Tissue was dehydrated in graded alcohol, treated with propylene oxide and embedded in epoxy resin (EMix). Thin sections were stained with uranyl acetate and lead citrate, and examined in a Jeol 100 CX electron microscope. Samples of the tumour were also snap-frozen in liquid nitrogen and then stored at -220C for cytostate sectioning. Several antigenic determinants were sought in cryostat sections of the lesions after the application of monoclonal antibodies listed in Table I. These antibodies were derived from the Third and Fourth Workshops on Human Leucocyte Differentiation Antigens (Hogg & Horton, 1987;Knapp et al., 1989). Immunohistochemistry was performed using an indirect immunoperoxidase technique (Gatter et al., 1984).Preparation of isolated macrophages and macrophage polykaryons The remainder of the tissue was...

show abstract

“…The synovial microvascular endothelial cell undergoes marked phenotypic alterations in RA, including up-regulation of leukocyte adhesion proteins and immunoreactive COX staining, as well as morphologic alterations in thickness and ultrastructure (17)(18)(19). These changes correlate with well-characterized, cytokine-mediated activation responses of human urn-bilical vein endothelial cells in vitro (20).…”

mentioning

confidence: 99%

Induction of cyclooxygenase ii in human synovial microvessel endothelial cells by interleukin‐1

Szczepanski

Moatter

Carley

et al. 1994

Arthritis & Rheumatism

View full text Add to dashboard Cite

Objective. To characterize the effects of interleukin-la (IL-1) on prostanoid biosynthesis by human rheumatoid synovium microvessel endothelium (HSE).Methods. HSE cells were treated with cytokines, metabolic inhibitors, and steroids under various conditions, and prostaglandin biosynthesis was determined by radioimmunoassay. Newly synthesized cyclooxygenase (COX) was quantitated by immunoprecipitation of metabolically labeled HSE cell lysates. The effects of IL-1 on levels of messenger RNA (mRNA) for COX I1 were also determined.Results. IL-1 induced an increase in COX activity (as assessed by prostaglandin E, release) that was doseand time-dependent and was blocked by cycloheximide, actinomycin D, and dexamethasone. IL-1 induced a selective increase in COX I1 mRNA and biosynthesis of COX I1 protein that was blocked by dexamethasone.Conclusion. IL-1 treatment of HSE cells induces COX 11, as demonstrated by both Northern blotting and immunoprecipitation. The induction of COX I1 expression provides, at least in part, a mechanism for the pronounced increase in prostanoid synthesis observed in HSE cells following incubation with IL-1. The selective up-regulation of HSE COX I1 by inflammatory cytokines such as IL-1 suggests that development of specific pharmaceutical inhibitors for this novel isozyme may

show abstract

Immunohistologic analysis of the distribution of cell adhesion molecules within the inflammatory synovial microenvironment

Cited by 181 publications

References 44 publications

Role of cytokines in inflammatory synovitis

Role of cytokines in inflammatory synovitis

Bone resorption by macrophage polykaryons of giant cell tumour of tendon sheath

Induction of cyclooxygenase ii in human synovial microvessel endothelial cells by interleukin‐1

Contact Info

Product

Resources

About