title: Expression and function of surface antigens on scleroderma fibroblasts.
abstract: 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-1 alpha, tumor necrosis factor alpha, and interferon-gamma. 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.
authors.affiliation: Cell Enzymology Unit, Mathilda and Terence Kennedy Institute of Rheumatology, Hammersmith, London, England.
authors.forename: D
authors.initials: D
authors.lastname: Abraham
authors.forename: S
authors.initials: S
authors.lastname: Lupoli
authors.forename: A
authors.initials: A
authors.lastname: McWhirter
authors.forename: C
authors.initials: C
authors.lastname: Plater-Zyberk
authors.forename: T H
authors.initials: TH
authors.lastname: Piela
authors.forename: J H
authors.initials: JH
authors.lastname: Korn
authors.forename: I
authors.initials: I
authors.lastname: Olsen
authors.forename: C
authors.initials: C
authors.lastname: Black
mesh_terms: D000328:Adult; D000368:Aged; D000911:Antibodies, Monoclonal / Q000276:immunology; D000945:Antigens, Differentiation, T-Lymphocyte / Q000276:immunology / Q000378:metabolism; D000954:Antigens, Surface / Q000235:genetics* / Q000276:immunology / Q000378:metabolism / Q000502:physiology; D018801:CD2 Antigens; D018968:CD58 Antigens; D002448:Cell Adhesion / Q000187:drug effects / Q000502:physiology; D015815:Cell Adhesion Molecules / Q000276:immunology / Q000378:metabolism; D005260:Female; D005347:Fibroblasts / Q000166:cytology / Q000276:immunology* / Q000473:pathology; D006801:Humans; D018799:Intercellular Adhesion Molecule-1; D007371:Interferon-gamma / Q000494:pharmacology; D007375:Interleukin-1 / Q000494:pharmacology; D008297:Male; D008562:Membrane Glycoproteins / Q000276:immunology / Q000378:metabolism; D008875:Middle Aged; D011971:Receptors, Immunologic / Q000276:immunology / Q000378:metabolism; D012595:Scleroderma, Systemic / Q000276:immunology* / Q000473:pathology / Q000503:physiopathology; D013601:T-Lymphocytes / Q000378:metabolism / Q000473:pathology / Q000502:physiology; D014409:Tumor Necrosis Factor-alpha / Q000494:pharmacology
chemical_list: D000911:Antibodies, Monoclonal; D000945:Antigens, Differentiation, T-Lymphocyte; D000954:Antigens, Surface; D018801:CD2 Antigens; D018968:CD58 Antigens; D015815:Cell Adhesion Molecules; D007375:Interleukin-1; D008562:Membrane Glycoproteins; D011971:Receptors, Immunologic; D014409:Tumor Necrosis Factor-alpha; D018799:Intercellular Adhesion Molecule-1; D007371:Interferon-gamma