Interaction of v-Ki-ras oncogene and interferon-γ in the control of histocompatibility antigen expression in mouse fibroblasts

Morris, Alan; Ward, GA; Bateman, W. J.

doi:10.1016/0008-8749(89)90214-1

Cited by 8 publications

(12 citation statements)

References 11 publications

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“…However, contrasting results have been presented for the effects of type I IFNs on MHC class II expression. Several reports indicate that type I IFNs do not induce class II expression by, for example, monocytes and melanomas (Houghton et al, 1984;Kelley, Fiers & Strom, 1984;Basham & Merigan, 1983) as well as epithelial cells like thyrocytes (Todd et al, 1985;Weetman et al, 1985) Furthermore, consistent with our studies reported here, it has been found that type I IFNs inhibit IFN-y-mediated enhancement of class II expression in murine macrophages (Ling, Warren & Vogel, 1985;Inaba et al, 1986), fibroblasts and glial cells (Morris & Tomkins, 1989), and in human endothelial cells (Lapierre, Fiers & Pober, 1988). By contrast, others have reported type I IFNs to stimulate class II expression by melanoma and lymphoblastoid cell lines (Dolei, Capobiancho & Ameglio, 1983;Giacomini et al, 1984), but that this effect was slight, and certainly much less than that of IFN-y.…”

Section: Discussionsupporting

confidence: 82%

“…Activation of leucocytes and/ or destruction of thyrocytes in autoimmune thyroiditis could itself lead to increased levels of these modulators in the thyroid, and so exacerbate the pathogenesis (Pujol-Borrell & Todd, 1987). However, EGF and TGF-a suppress class II induction in thyrocytes by IFN-y (Todd et al, 1987a(Todd et al, , 1990 (Morris & Tomkins, 1989). Consistent with our own findings, Morris & Tomkins (1989) suggest that high levels of type I IFNs induced during viral infections may inhibit inappropriate induction of MHC class II by IFN-y derived from T cells responding to the virus, thus possibly inhibiting the development of autoimmune responses.…”

Section: Discussionsupporting

confidence: 80%

“…Of particular relevance in the present context are the findings of Rhodes et al (1986) who showed that whereas rIFN-ac2 has no effect on HLA class II by human monocytes, rIFN-cxl increases class II expression by these cells. However, Morris & Tomkins (1989) found that rIFN-a2 (unlike natural IFN- (Todd et al, 1987a(Todd et al, , 1990. In contrast, Acres, Lamb & Feldmann (1985) reported EGF to enhance class II expression by peripheral blood antigen-presenting cells.…”

Section: Discussionmentioning

confidence: 99%

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Suppression of HLA class II expression on thyrocytes by interferon-alpha 1

Guerin¹,

Todd²,

Hammond³

et al. 1990

Clinical and Experimental Immunology

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Section: Discussionsupporting

confidence: 82%

Section: Discussionsupporting

confidence: 80%

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Suppression of HLA class II expression on thyrocytes by interferon-alpha 1

Guerin¹,

Todd²,

Hammond³

et al. 1990

Clinical and Experimental Immunology

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“…To confirm that an open reading frame was maintained, the DNA sequences at the junction between promoter and the p-gal gene were verified using a primer specific for the GFAP promoter. The construct was tested by transient transfections, according to calcium phosphate method (Hanahan, 1985) in mouse astrocytes primary culture (Morris and Tompkins, 1989). Promoter activity was revealed 48 h after in 2 mM X-gal at 31°C.…”

Section: Materials and Methods Transgene Constructionmentioning

confidence: 99%

Normal and pathological expression of GFAP promoter elements in transgenic mice

Galou

Pournin

Ensergueix

et al. 1994

Glia

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The expression of the glial fibrillary acidic protein (GFAP), a component of astroglial intermediate filaments, is regulated under developmental and pathological conditions. In order to characterize DNA sequences involved in such regulations, we produced transgenic mice bearing 2 kb of the 5' flanking region of the murine GFAP gene linked to the Escherichia coli beta-galactosidase (beta-gal) reporter gene. Seven transgenic lines were obtained. We observed that the regulatory elements present in the transgene GFAP-nls-LacZ direct an expression in the neural and non-neural tissue and target in vivo an unexpected subpopulation of astrocyte. In the developing brain, beta-gal activity and GFAP appeared simultaneously and in the same region, on embryonic day 18 (E18), suggesting that the 2 kb of the promoter contains the regulatory sequences responsible for the perinatal vimentin/GFAP switch. In addition, we demonstrated that the 2 kb sequence of the GFAP promoter used in the transgene possess elements which are activated after a surgical injury, thus permitting to study some aspects of reactive gliosis in these transgenic mice. These transgenic lines provide a useful tool by enabling further studies of astroglial and, probably, neuronal physiologies.

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“…It may be that the constitutive expression of class I antigen is a major determinant of tumorigenicity in this system; in which case, to study a potential role for induced class II antigens we should choose class I-negative clones and determine whether there is then a correlation of class II inducibility with lower tumorigenicity. An alternative strategy that we are currently pursuing is to sort (by fluorescence activated cell sorter) sublines which differ in their inducibility for class II but otherwise have similar MHC phenotypes (Morris et al, 1989); these in preliminary experiments do appear to differ in their tumorigenicity, with the more inducible subline being less tumorigenic. Of course, there must be many factors which influence the ability of cells expressing activated ras to grow as a tumour, and it is at present impossible to determine whether instability of MHC antigen expression, either constitutive or induced, is of decisive importance.…”

Section: Methodsmentioning

confidence: 99%

Instability of expression of major histocompatibility antigens in fibroblasts expressing activated ras oncogene: constitutive and interferon-gamma induced class I and class II antigens in a series of clonal isolates of murine fibroblasts transformed by v-Ki-ras

Morris

Ward²,

Bateman³

1989

Br J Cancer

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SummaryWe have examined the expression of major histocompatibility complex (MHC) antigens, constitutive or induced with interferon gamma (IFN-y), in a line of C3H mouse embryo fibroblasts (C3H 2.01) transformed with a helper-virus-free preparation of the Kirsten strain of murine sarcoma virus. C3H201 cells expressed some class I antigen (H-2Kk) in the absence of added interferon, unlike the parental C3H lOT1/2 cells from which they were derived. However, this declined with (in vitro) passage level after transformation. Treatment with IFN-y induced very high expression of H-2Kk at all passage levels. There was no constitutive expression of class II antigen (I-Ak); however, this could be induced by IFN-y. Inducibility of I-Ak was found also to be related to the number of passages after transformation; at early passage levels after transformation more I-Ak was induced than after the cells had been allowed to grow for several passages, until at high passage levels little or no I-Ak was induced. This was not due to the presence of a subpopulation of untransformed cells since when the cells were cloned shortly after infection all the resulting clones were transformed. In addition, IFN-y at any passage level induced clearly less I-Ak than was found in C3H lOT1/2 cells, in which I-Ak inducibility was high and stable. Twenty-one clones were derived from C3H 201 cells at early passage (<8) either from soft agar or from liquid culture. These clones showed a wide variation in MHC antigen phenotype. Many expressed H-2Kk in the absence of IFN-y, and all were strongly inducible for H-2Kk. None showed I-Ak in the absence of IFN-y. All but two expressed I-Ak after IFN-y treatment but, with four exceptions, clearly less than the untransformed line. Four clones derived at late passage (40) resembled the late passage line. The expression of the ras oncogene and tumorigenicity was studied in representative clones; there was no obvious correlation with MHC phenotype, nor with the method of cloning. We conclude from these studies that the expression of MHC antigens by fibroblasts expressing the vKi-ras oncogene, either with or without exposure to interferon gamma, is unstable, varying with the number of cell generations from transformation and from clone to clone.

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Interaction of v-Ki-ras oncogene and interferon-γ in the control of histocompatibility antigen expression in mouse fibroblasts

Cited by 8 publications

References 11 publications

Suppression of HLA class II expression on thyrocytes by interferon-alpha 1

Suppression of HLA class II expression on thyrocytes by interferon-alpha 1

Normal and pathological expression of GFAP promoter elements in transgenic mice

Instability of expression of major histocompatibility antigens in fibroblasts expressing activated ras oncogene: constitutive and interferon-gamma induced class I and class II antigens in a series of clonal isolates of murine fibroblasts transformed by v-Ki-ras

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