Summary
A major factor in cellular cytotoxicity is the interaction between LFA-1 on leukocytes and ICAM-1 on targets. Because several inflammatory cartilage diseases are characterized by the presence of leukocyte infiltrates, the expression of ICAM-1 on human cartilage, cultured chondrocytes, and transplanted cartilage was investigated using monoclonal antibodies. Frozen tissue sections, chondrocytes in suspension, as well as total cellular mRNA were prepared from human cartilage samples. ICAM-1 expression was studied with two different monoclonal antibodies directed against ICAM-1 by immunohistochemical APAAP-staining and additional flow cytometric analyses. The expression of ICAM-1-mRNA in cartilage tissue was analyzed using the northern blot hybridization technique. Furthermore, chondrocytes were treated in culture with interleukin-1 (IL-1) and gamma-interferon (gamma-IFN). ICAM-1 expression after culture was quantified using flow cytometric analysis. We could detect ICAM-1 mRNA in cartilage tissue, however, the immunostaining of tissue sections using monoclonal antibodies did not give clear positive reactions. Isolated chondrocytes showed strongly positive staining patterns in comparison with adequate negative controls as assessed by flow cytometry. A dose-dependent increase of the expression of ICAM-1 on chondrocytes was observed when stimulated with IL-1 and gamma-IFN. Finally, two of the three studied transplanted autologous cartilage samples with advanced resorption showed the presence of ICAM-1 molecules as assessed by immunohistochemistry. This expression of ICAM-1 suggests that the molecule plays a role in severe cartilage inflammatory processes, where tissue damage leads to the exposure of chondrocyte surfaces.
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Alsalameh, S.; Jahn, B.; Krause, A., et al. Antigenicity and accessory cell function of class-II-positive human nasal chondrocytes. J. Rheumatol. 18:414–421; 1991.
Boyd, A. W.; Wawryk, S. O.; Burn, G. F. ICAM-1 has a central role in cell-cell contact-mediated immune mechanisms. Proc. Natl. Acad. Sci. USA 85:3095–3099; 1988.
Bujía, J.; Alsalameh, S.; Naumann, A., et al. Humoral immune response against minor collagens type IX and XI in patients with cartilage graft resorption after reconstructive surgery. Ann. Rheum. Dis. 53:229–234; 1994a.
Bujía, J.; Alsalameh, S.; Sittinger, M., et al. Antigen presenting cell function of class-II-positive human nasal chondrocytes. Acta Oto-Laryngol. 114:75–79; 1994b.
Bujía, J.; Pitzke, P.; Hammer, C., et al. Culture and cryopreservation of chondrocytes from human cartilage: relevance for cartilage allografting in otolaryngology. ORL 54:80–84; 1992b.
Bujía, J.; Wilmes, E.; Hammer, C., et al. Class II antigen induction in cartilage. Ann. Rheum. Dis. 51:1098–1099; 1992a.
Bujía, J.; Wilmes, E.; Krombach, F., et al. Detection of class II antigens on human nasal cartilage. Am. J. Otolaryngol. 11:339–344; 1990a.
Bujía, J.; Wilmes, E.; Krombach, F., et al. The effect of gamma interferon on HLA class II antigen expression on isolated human nasal chondrocytes. Eur. Arch. Oto-Rhino-Laryngol. 247:287–290; 1990b.
Burmester, G. R.; Menche, D.; Merryman, P. Application of monoclonal antibodies to the characterization of cells eluted from human articular cartilage. Expression of Ia antigens in certain diseases and identification of an 85-kD cell surface molecule accumulated in the peri-cellular matrix. Arthritis Rheum. 26:1187–1195; 1983.
Chiang, M. Y.; Chang, H.; Zouner, M. A., et al. Antisense oligonucleotides inhibit intercellular adhesion molecule 1 expression by two distinct mechanisms. J. Biol. Chem. 266:18162–18171; 1991.
Chirgwin, J.; Przybyla, A.; McDonald, R., et al. Isolation of biologically active ribonucleic acid from sources enriched in ribonuclease. Biochemistry 18:5294–5299; 1979.
Davies, M. E.; Dingle, J. T.; Pigott, R., et al. Expression of ICAM-1 on human articular cartilage chondrocytes. Connect. Tissue Res. 26:207–216; 1991a.
Davies, M. E.; Horner, A.; Dingle, J. T. Immune recognition of chondrocytes in articular cartilage activated by synovial interleukin-1. Connect. Tissue Res. 25:243–239; 1991b.
Dingle, J. T.; Davies, M. E.; Mativi, B. Y., et al. Immunohistological identification of IL-1 activated chondrocytes. Ann. Rheum. Dis. 49:889–892; 1990.
Dustin, M. L.; Tohlein, R.; Bhan, A. K. Induction of IL-1 and IFN-gamma: tissue distribution, biochemistry and function of a natural adherence molecule (ICAM-1). J. Immunol. 137:245–254; 1986.
Gerritsen, M. E.; Kelley, K. A.; Ligon, G., et al. Regulation of the expression of ICAM-1 in cultured human endothelial cells derived from rheumatoid synovium. Arthritis Rheum. 36:593–602; 1993.
Gibbs, V. C.; Wood, D. M.; Garovoy, R. G. The response of cultured human kidney capillary endothelium to immunologic stimuli. Hum. Immunol. 15:259–269; 1985.
Hirschberg, H.; Bergh, O. J.; Thorsby, E. Antigen presentation by vascular endothelial cells and epidermal Langerhans cells: the role of HLA-DR. Immunol. Rev. 66:57–77; 1982.
Jahn, B.; Burmester, G. R.; Schmidt, H. Changes in cell surface antigen expression on human articular chondrocytes induced by gamma-interferon. Induction of Ia antigens. Arthritis Rheum. 30:64–74; 1987.
Kurzinger, K.; Reynolds, T.; Germain, R. N., et al. A novel lymphocyte function associated antigen (LFA-1): cellular distribution, quantitative expression and structure. J. Immunol. 127:596–602; 1981.
Kvale, D.; Krajii, P.; Brandtzyog, P. Expression and regulation of adhesion molecules ICAM-1 (CD54) and LFA-3 (CD58) in human epithelial cell lines. Scand. J. Immunol. 35:669–676; 1992.
Makgoba, M. W.; Sanders, M. E.; Ginther Luce, G. E. ICAM-1 is a ligand for LFA-1 dependent adhesion of B, T and myeloid cells. Nature 331:86–91; 1988a.
Makgoba, M. W.; Sanders, M. E.; Luce, G. E. Functional evidence that intercellular adhesion molecule-1 (ICAM-1) is a ligand for LFA-1 adhesion in T cell mediated cytotoxicity. Eur. J. Immunol. 18:637–640; 1988b.
Marlin, S. D.; Pringer, T. A. Purified intercellular adhesion molecule-1 (ICAM-1) is a ligand for lymphocyte function associated antigen-1 (LFA-1). Cell 51:813–819; 1987.
Montefort, S.; Holgate, S. T. Adhesion molecules and their role in inflammation. Respir. Med. 85:91–99; 1991.
Pitzke, P.; Bujía, J.; Wilmes, E., et al. Expression of ICAM-1 on isolated human nasal, auricular and costal chondrocytes. Acta Oto-Laryngol. 114:81–86; 1994.
Rath, N. C.; Oronsky, A. L.; Kerwar, S. S. Synthesis of interleukin-1-like activity by normal rat chondrocytes in culture. Clin. Immunol. Immunopathol. 47:39–46; 1988.
Schwable, W.; Kerstin, M.; Meyer Zum Büschenfelde, K. M., et al. De novo expression of ICAM-1 in pancreas cancer. Int. J. Cancer 53:328–333; 1993.
Simmons, D.; Makgoba, M. W.; Seed, B. ICAM: an adhesion ligand of LFA-1, is homologous to the neural cell adhesion molecule NCAM. Nature 331:624–627; 1988.
Staunton, D. E.; Marlin, S. D.; Stratona, C., et al. Primary structure of ICAM-1 demonstrates interactions between members of the immunoglobulin and integrin supergene family. Cell 52:925–933; 1988.
Tiku, M. L.; Lui, S.; Weaver, C. W., et al. Class II histocompatibility antigen-mediated immunologic function of normal articular chondrocytes. J. Immunol. 135:2912–2918; 1985.
Voraberger, G.; Schäfer, R.; Stratowa, C. Cloning of the human gene for ICAM-1 and analysis of its 5′-regulatory region. J. Immunol. 147:2777–2786; 1991.
Von Der Mark, K.; Gauss, B.; Von Der Mark, H., et al. Relationship between shape and type of collagen synthesized as chondrocytes lose their cartilage phenotype in culture. Nature 267:531–532; 1977.
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Bujia, J., Behrends, U., Rotter, N. et al. Expression of ICAM-1 on intact cartilage and isolated chondrocytes. In Vitro Cell.Dev.Biol.-Animal 32, 116–122 (1996). https://doi.org/10.1007/BF02723043
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DOI: https://doi.org/10.1007/BF02723043