Expression and Function of Surface Antigens on Scleroderma Fibroblasts
D. Abraham PhD
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorS. Lupoli MD
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorA. McWhirter BSc.
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorC. Plater-Zyberk PhD
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorT. H. Piela PhD
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorJ. H. Korn MD
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorCorresponding Author
Irwin Olsen PhD
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Address reprint requests to Irwin Olsen, PhD, Cell Enzymology Unit, The Mathilda and Terence Kennedy Institute of Rheumatology, 6 Bute Gardens, Hammersmith, London W6 7DW, UKSearch for more papers by this authorC. Black
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorD. Abraham PhD
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorS. Lupoli MD
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorA. McWhirter BSc.
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorC. Plater-Zyberk PhD
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorT. H. Piela PhD
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorJ. H. Korn MD
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorCorresponding Author
Irwin Olsen PhD
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Address reprint requests to Irwin Olsen, PhD, Cell Enzymology Unit, The Mathilda and Terence Kennedy Institute of Rheumatology, 6 Bute Gardens, Hammersmith, London W6 7DW, UKSearch for more papers by this authorC. Black
From the Cell Enzymology Unit and the Division of Clinical Immunology, The Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, the Department of Rheumatology, Royal Free Hospital Medical School, London, England, and the Veterans Administration Medical Center and University of Connecticut School of Medicine, Newington
Search for more papers by this authorAbstract
Dermal fibroblasts from patients with systemic sclerosis (SSc) bound a much greater number of T lymphocytes than did normal dermal fibroblasts. Monoclonal antibodies (MAb) against classes I and II antigens of the major histocompatibility complex (MHC) and their receptors, CD8 and CD4, had no effect on T cell interaction with SSc and normal cells, while MAb against lymphocyte function–associated antigen type 3 (LFA-3) and CD2 both strongly inhibited lymphocyte attachment. MAb against intercellular adhesion molecule type 1 (ICAM-1) and LFA-1 also prevented binding of T lymphocytes, but had a more marked effect on adhesion to SSc fibroblasts than to normal fibroblasts; they also completely abolished the increased binding to fibroblasts treated with interleukin-1α, tumor necrosis factor α, and interferon-γ. No difference was found in the proportion of normal and SSc fibroblasts that expressed MHC classes I and II and LFA-3, but more SSc cells expressed ICAM-1, and at a higher level, than did normal fibroblasts. These results show that cultured SSc cells have elevated binding to T lymphocytes, which possibly results from expansion of a subset of fibroblasts that produces high levels of ICAM-1.
References
- 1 Rodnan GP, Lipinski E, Luksick J: Skin thickness and collagen content in progressive systemic sclerosis and localized scleroderma. Arthritis Rheum 22: 130–140, 1979
- 2 LeRoy EC: The connective tissue in scleroderma. Coll Relat Res 1: 301–308, 1981
- 3 Black C, Myers AR: Current Topics in Rheumatology: Systemic Sclerosis: Scleroderma, International Conference on Progressive Systemic Sclerosis, Austin, Texas, October 20–23, 1981. New York, Gower, 1985
- 4 Bailey AJ, Black CM: The role of connective tissue in the pathogenesis of scleroderma, Systemic Sclerosis: Scleroderma. Edited by MIV Jayson, CM Black. New York, John Wiley & Sons, 1988
- 5 MIV Jayson, CM Black, editors: Systemic Sclerosis: Scleroderma. New York, John Wiley & Sons, 1988
- 6 Mauch C, Krieg T: Fibroblast and matrix interactions and their role in the pathogenesis of fibrosis. Rheum Dis Clin North Am 16: 93–107, 1990
- 7 Black CM, editor: Raynaud's phenomenon, scleroderma, overlap syndromes and other fibrosing syndromes. Curr Opin Rheumatol 1: 473–528, 1989
- 8 Needleman BW, Ordonez JV, Taramelli D, Alms W, Gayer K, Choi J: In vitro identification of a subpopulation of fibroblasts that produces high levels of collagen in scleroderma patients. Arthritis Rheum 33: 842–852, 1990
- 9 Uitto J, Bauer EA, Eisen AZ: Scleroderma: increased biosynthesis of triple-helical type I and type III procollagens associated with unaltered expression of collagenase by skin fibroblasts. J Clin Invest 64: 921–930, 1979
- 10 LeRoy EC: Collagen deposition in autoimmune diseases: the expanding role of the fibroblast in human fibrotic disease. Ciba Found Symp 114: 196–207, 1985
- 11 Whiteside TL, Ferrarini M, Hebda P, Buckingham RB: Heterogeneous synthetic phenotype of cloned scleroderma fibroblasts may be due to aberrant regulation in the synthesis of connective tissues. Arthritis Rheum 31: 1221–1229, 1988
- 12 Jimenez SA, Feldman G, Bashey RI, Bienkowski R, Rosenbloom J: Co-ordinate increase in the expression of type I and type III collagen genes in progressive systemic sclerosis fibroblast. Biochem J 237: 837–843, 1986
- 13 Vuorio T, Makela JK, Vuorio E: Activation of type I collagen genes in cultured scleroderma fibroblasts. J Cell Biochem 28: 105–113, 1985
- 14 Kahari VM, Sandberg M, Vuorio T, Vuorio E: Identification of fibroblasts responsible for increased collagen production in localized scleroderma by in situ hybridization. J Invest Dermatol 90: 664–670, 1988
- 15 Scharffetter K, Lankat-Buttgereit B, Krieg T: Localization of collagen mRNA in normal and scleroderma skin by in situ hybridization. J Clin Invest 18: 9–17, 1988
- 16 Fleischmajer R, Perlish JS, Reeves JRT: Cellular infiltrates in scleroderma skin. Arthritis Rheum 20: 975–984, 1977
- 17 Gustafsson R, Totterman TH, Klareskog L, Hallgren R: Increase in activated T cells and reduction in suppressor inducer T cells in systemic sclerosis. Ann Rheum Dis 49: 40–45, 1990
- 18 Ferrarini M, Steen V, Medsger TA Jr, Whiteside TL: Functional and phenotypic analysis of T lymphocytes cloned from the skin of patients with systemic sclerosis. Clin Exp Immunol 79: 346–352, 1990
- 19 Van de Water J, Haapanen L, Boyd R, Abplanalp H, Gershwin ME: Identification of T cells in early dermal lymphocytic infiltrates in avian scleroderma. Arthritis Rheum 32: 1031–1040, 1989
- 20 Umehara H, Kumagai S, Murakami M, Suginoshita T, Tanaka K, Hashida S, Ishikawa E, Imura H: Enhanced production of interleukin-1 and tumor necrosis factor α by cultured peripheral blood monocytes from patients with scleroderma. Arthritis Rheum 33: 893–897, 1990
- 21 LeRoy EC, Smith EA, Kahaleh MB, Trojanowska M, Silver RM: A strategy for determining the pathogenesis of systemic sclerosis: is transforming growth factor β the answer? Arthritis Rheum 32: 817–825, 1989
- 22 Gruschwitz M, Muller PU, Sepp N, Hofer E, Fontana A, Wick G: Transcription and expression of transforming growth factor type beta in the skin of progressive systemic sclerosis: a mediator of fibrosis? J Invest Dermatol 94: 197–203, 1990
- 23 Julius MH, Simpson E, Herzenberg LA: A rapid method for the isolation of functional thymus-derived murine lymphocytes. Eur J Immunol 3: 645–649, 1975
- 24 Rennard SI, Berg R, Martin GR, Foidart JM, Robey PG: Enzyme-linked immunoassay (ELISA) for connective tissue components. Anal Biochem 104: 205–214, 1980
- 25 Piela TH, Korn JH: ICAM-1-dependent fibroblast-lymphocyte adhesion: discordance between surface expression and function of ICAM-1. Cell Immunol 129: 125–137, 1990
- 26 Springer TA: Adhesion receptors of the immune system. Nature 346: 425–434, 1990
- 27 Altman DM, Hogg N, Trowsdale J, Wilkinson D: Cotransfection of ICAM-1 and HLA-DR reconstitutes human antigen-presenting cell function in mouse L cells. Nature 338: 512–514, 1989
- 28 Makgoba MW, Sanders ME, Ginther Luce GE, Dustin ML, Springer TA, Clark EA, Mannoni P, Shaw S: ICAM-1, a ligand for LFA-1-dependent adhesion of B, T and myeloid cells. Nature 331: 86–88, 1988
- 29 Siu G, Hedrick SM, Brian AA: Isolation of the murine intercellular adhesion molecule-1 (ICAM-1) gene: ICAM-1 enhances antigen-specific T cell activation. J Immunol 143: 3813–3820, 1987
- 30 Springer TA, Dustin ML, Kishimoto TK, Marlin SD: The lymphocyte function-associated LFA-1, CD2, and LFA-3 molecules: cell adhesion receptors of the immune system. Annu Rev Immunol 5: 223–252, 1987
- 31 Postlethwaite AE, Stuart JM, Kang AH: The cell-mediated immune system in progressive systemic sclerosis: an overview. International Conference on Progressive Systemic Sclerosis, Austin, Texas, October 20–23, 1981. New York, Gower, 1985
- 32 Abraham D, Muir H, Olsen I: Fibroblast matrix and surface components that mediate cell-to-cell interaction with lymphocytes. J Invest Dermatol 93: 335–340, 1989
- 33 Vollger LW, Tuck DT, Springer TA, Haynes BF, Singer KH: Thymocyte binding to human thymic epithelial cells is inhibited by monoclonal antibodies to CD2 and LFA-3 antigens. J Immunol 138: 353–363, 1987
- 34 Clark JG, Dedon TF, Wayner EA, Carter WG: Effects of interferon-γ on expression of cell surface receptors for collagen and deposition of newly synthesized collagen by cultured human lung fibroblasts. J Clin Invest 83: 1505–1511, 1989
- 35 Amento EP, editor: Connective tissue metabolism including cytokines. Curr Opin Rheumatol 1: 485–489, 1989
- 36 Dustin ML, Singer KH, Tuck DT, Springer TA: Adhesion of T lymphoblasts to epidermal keratinocytes is regulated by interferon γ and is mediated by intercellular adhesion molecule-1 (ICAM-1). J Exp Med 167: 1323–1340, 1988
- 37 Dustin ML, Rothlein R, Bahn AK, Dinarello CA, Springer TA: Induction by IL-1 and interferon-γ: tissue distribution, biochemistry, and function of a natural adherence molecule (ICAM-1). J Immunol 137: 245–254, 1986
- 38 Piela TH, Korn JH: Lymphocyte-fibroblast adhesion induced by interferon-gamma. Cell Immunol 114: 149–160, 1988
- 39 Abraham D, Bokth S, Bou-Gharios G, Beauchamp J, Olsen I: Interactions between lymphocytes and dermal fibroblasts: an in vitro model of cutaneous lymphocyte trafficking. Exp Cell Res 190: 118–126, 1990
- 40 Griffiths CEM, Voorhees JJ, Nickoloff BJ: Gamma interferon induces different keratinocyte cellular patterns of expression of HLA-DR and DQ and intercellular adhesion molecule-1 (ICAM-1) antigens. Br J Dermatol 120: 1–7, 1989
- 41 Frohman EM, Frohman TC, Dustin ML, Vayuvegula B, Choi B, Gupta A, van der Noort S, Gupta S: The induction of intercellular adhesion molecule 1 (ICAM-1) expression on human fetal astrocytes by interferongamma, tumour necrosis factor α, lymphotoxin and interleukin-1: relevance to intracerebral antigen presentation. J Neuroimmunol 23: 117–124, 1989
- 42 Rothlein R, Czajkowski M, O'Neill MM, Marlin SD, Mainolfi E, Merluzzi VJ: Induction of intercellular adhesion molecule 1 on primary and continuous cell lines by pro-inflammatory cytokines: regulation by pharmacologic agents and neutralizing antibodies. J Immunol 141: 1665–1669, 1988
- 43 Beauchamp JR, Abraham DJ, Bou-Gharios G, Partridge TA, Olsen I: Expression and function of heterotypic adhesion molecules during differentiation of human skeletal muscle in culture. Submitted for publication
- 44 Wantzin GL, Ralfkiaer E, Steen L, Rothlein R: The role of intercellular adhesion molecules in inflammatory skin reactions. Br J Dermatol 119: 141–145, 1988
- 45 Krieg T, Perlish J, Fleischmajer R, Braun-Falco O: Collagen synthesis in scleroderma: selection of fibroblast populations during subcultures. Arch Dermatol Res 277: 373–376, 1985
- 46 Botstein GR, Sherer GK, LeRoy EC: Fibroblast selection in scleroderma: an alternative model of fibrosis. Arthritis Rheum 25: 189–195, 1982
- 47 Maxwell DB, Grotendorst CA, Grotendorst GR, LeRoy EC: Fibroblast heterogeneity in scleroderma: C1q studies. J Rheumatol 14: 756–759, 1987
- 48 Korn JH, Halushka PV, LeRoy EC: Mononuclear cell modulation of connective tissue function: suppression of fibroblast growth by stimulation of endogenous prostaglandin production. J Clin Invest 65: 543–554, 1980
- 49 Needleman BW: Increased expression of intercellular adhesion molecule 1 on the fibroblasts of scleroderma patients. Arthritis Rheum 33: 1847–1851, 1990
