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MHC class II antigen expression in human vascular smooth muscle cells is induced by interferon-gamma and modulated by tumour necrosis factor and lymphotoxin.
Immunology. 1990 Feb; 69(2):243-9.I

Abstract

Arterial smooth muscle cells (SMC) express major histocompatibility complex (MHC) class II antigens in experimental vasculitis and in the human atherosclerotic plaque. We have therefore studied the regulation of expression of MHC antigens in cultured human arterial SMC, using immunofluorescence, radioimmunoprecipitation and a quantitative cell-surface immunoradiometric assay. SMC expressed class I, but not class II, antigens on their cell surfaces under basal conditions. Treatment of SMC with recombinant or natural interferon-gamma (IFN-gamma) induced expression of class II antigens in the following order of intensity, DR greater than DP greater than DQ. HLA-DR protein in SMC showed the same MW as that synthesized by B-lymphoblastoid cells. Antibodies to IFN-gamma blocked all HLA-DR-inducing activity in mixed leucocyte reaction (MLR) supernatants and PHA-stimulated peripheral blood mononuclear cell (PBMC)-conditioned media, indicating that IFN-gamma is the only lymphokine secreted under these conditions that is capable of de novo induction of HLA-DR expression in SMC. Treatment of SMC with recombinant human tumour necrosis factor-alpha (TNF) or lymphotoxin (LT) did not per se induce class II antigen expression. However, both TNF and LT substantially enhanced IFN-gamma-induced expression of HLA-DQ while decreasing that of HLA-DP. TNF, but not LT, increased HLA-DR expression. Also, in dermal fibroblasts, IFN-gamma-induced HLA-DP expression was significantly inhibited in the presence of TNF. These data demonstrate that TNF and LT differentially modulate IFN-gamma-induced MHC antigen expression in mesenchymal cells. The fact that SMC can express MHC class II antigens suggests that this cell type may serve as an accessory cell in the initiation of the immune response.

Authors+Show Affiliations

Department of Clinical Chemistry, Gothenburg University, Sweden.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

2106484

Citation

Stemme, S, et al. "MHC Class II Antigen Expression in Human Vascular Smooth Muscle Cells Is Induced By Interferon-gamma and Modulated By Tumour Necrosis Factor and Lymphotoxin." Immunology, vol. 69, no. 2, 1990, pp. 243-9.
Stemme S, Fager G, Hansson GK. MHC class II antigen expression in human vascular smooth muscle cells is induced by interferon-gamma and modulated by tumour necrosis factor and lymphotoxin. Immunology. 1990;69(2):243-9.
Stemme, S., Fager, G., & Hansson, G. K. (1990). MHC class II antigen expression in human vascular smooth muscle cells is induced by interferon-gamma and modulated by tumour necrosis factor and lymphotoxin. Immunology, 69(2), 243-9.
Stemme S, Fager G, Hansson GK. MHC Class II Antigen Expression in Human Vascular Smooth Muscle Cells Is Induced By Interferon-gamma and Modulated By Tumour Necrosis Factor and Lymphotoxin. Immunology. 1990;69(2):243-9. PubMed PMID: 2106484.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - MHC class II antigen expression in human vascular smooth muscle cells is induced by interferon-gamma and modulated by tumour necrosis factor and lymphotoxin. AU - Stemme,S, AU - Fager,G, AU - Hansson,G K, PY - 1990/2/1/pubmed PY - 1990/2/1/medline PY - 1990/2/1/entrez SP - 243 EP - 9 JF - Immunology JO - Immunology VL - 69 IS - 2 N2 - Arterial smooth muscle cells (SMC) express major histocompatibility complex (MHC) class II antigens in experimental vasculitis and in the human atherosclerotic plaque. We have therefore studied the regulation of expression of MHC antigens in cultured human arterial SMC, using immunofluorescence, radioimmunoprecipitation and a quantitative cell-surface immunoradiometric assay. SMC expressed class I, but not class II, antigens on their cell surfaces under basal conditions. Treatment of SMC with recombinant or natural interferon-gamma (IFN-gamma) induced expression of class II antigens in the following order of intensity, DR greater than DP greater than DQ. HLA-DR protein in SMC showed the same MW as that synthesized by B-lymphoblastoid cells. Antibodies to IFN-gamma blocked all HLA-DR-inducing activity in mixed leucocyte reaction (MLR) supernatants and PHA-stimulated peripheral blood mononuclear cell (PBMC)-conditioned media, indicating that IFN-gamma is the only lymphokine secreted under these conditions that is capable of de novo induction of HLA-DR expression in SMC. Treatment of SMC with recombinant human tumour necrosis factor-alpha (TNF) or lymphotoxin (LT) did not per se induce class II antigen expression. However, both TNF and LT substantially enhanced IFN-gamma-induced expression of HLA-DQ while decreasing that of HLA-DP. TNF, but not LT, increased HLA-DR expression. Also, in dermal fibroblasts, IFN-gamma-induced HLA-DP expression was significantly inhibited in the presence of TNF. These data demonstrate that TNF and LT differentially modulate IFN-gamma-induced MHC antigen expression in mesenchymal cells. The fact that SMC can express MHC class II antigens suggests that this cell type may serve as an accessory cell in the initiation of the immune response. SN - 0019-2805 UR - https://www.unboundmedicine.com/medline/citation/2106484/MHC_class_II_antigen_expression_in_human_vascular_smooth_muscle_cells_is_induced_by_interferon_gamma_and_modulated_by_tumour_necrosis_factor_and_lymphotoxin_ L2 - https://www.ncbi.nlm.nih.gov/pmc/articles/pmid/2106484/ DB - PRIME DP - Unbound Medicine ER -