Linkage of Mls genes to endogenous mammary tumour viruses of inbred mice

Frankel, Wayne N.; Rudy, Christine K.; Coffin, John M.; Huber, Brigitte

doi:10.1038/349526a0

Cited by 296 publications

(149 citation statements)

References 35 publications

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“…Expression of superantigens encoded by mouse mammary tumor viruses leads to I-E-dependent deletion of double-positive thymocytes bearing V␤5, 11, and 12 in B10.BR mice (27), and can be used as a model for negative selection. CD4 ϩ SP thymocytes from WT B10.BR and SHP2(CS) B10.BR mice were assessed for expression of V␤5, 11, and 12.…”

Section: T Cell Development In Shp2(cs) Micementioning

confidence: 99%

The src Homology 2 Domain-Containing Tyrosine Phosphatase 2 Regulates Primary T-Dependent Immune Responses and Th Cell Differentiation

Salmond

Huyer

Kotsoni

et al. 2005

The Journal of Immunology

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The src homology 2 domain-containing tyrosine phosphatase 2 (SHP2) plays an important role in development and in growth factor receptor signaling pathways, yet little is known of its role in the immune system. We generated mice expressing a dominant-negative version of the protein, SHP2(CS), specifically in T cells. In SHP2(CS) mice, T cell development appears normal with regard to both negative and positive selection. However, SHP2(CS) T cells express higher levels of activation markers, and aged mice have elevated serum Abs. This is associated with a marked increase in IL-4, IL-5, and IL-10 secretion by SHP2(CS) T cells in vitro. In addition, primary thymus-dependent B cell responses are deficient in SHP2(CS) mice. We show that whereas TCR-induced linker for activation of T cells phosphorylation is defective, CTLA-4 and programmed death-1 signaling are not affected by SHP2(CS) expression. Our results suggest that a key action of wild-type SHP2 is to suppress differentiation of T cells to the Th2 phenotype.

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Section: T Cell Development In Shp2(cs) Micementioning

confidence: 99%

The src Homology 2 Domain-Containing Tyrosine Phosphatase 2 Regulates Primary T-Dependent Immune Responses and Th Cell Differentiation

Salmond

Huyer

Kotsoni

et al. 2005

The Journal of Immunology

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“…Specific endogenous MMTV loci segregate with the deletion of certain specific classes of Tcells during the establishment of tolerance (Table 1) (Dyson et al, 1991;Frankel et al, 1991;Marrack et al, 1991 ;Woodland et al, 1991 a Janeway, 1991;Palmer, 1991 (Choi et al, 1991) in an in vitro assay. In the transgenic mouse study, the relevant T-lymphocyte subclass is deleted in response to the newly introduced superantigen , albeit at a slower rate than has been observed for normal endogenous Mls antigens.…”

Section: Mmtv and Superantigensmentioning

confidence: 99%

Factors controlling the expression of mouse mammary tumour virus

Günzburg

Salmons

1992

Biochemical Journal

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“…Retroviral superantigens were first depicted in the B-type virus group in mouse mammary tumor viruses and are found in both infectious mouse mammary tumor viruses and endogenous proviruses (14,18,39,63). It has been previously shown that the env gene of HERV-K18, a defective human endogenous provirus located on chromosome 1, encodes a superantigen activity (51,52).…”

mentioning

confidence: 99%

Epstein-Barr Virus Latent Membrane Protein LMP-2A Is Sufficient for Transactivation of the Human Endogenous Retrovirus HERV-K18 Superantigen

Sutkowski

Chen

Calderón

et al. 2004

J Virol

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Superantigens are microbial proteins that strongly stimulate T cells. We described previously that the Epstein-Barr virus (EBV) transactivates a superantigen encoded by the human endogenous retrovirus, HERV-K18. We now report that the transactivation is dependent upon the EBV latent cycle proteins. Moreover, LMP-2A is sufficient for induction of HERV-K18 superantigen activity.Superantigens are pathogen-derived proteins that elicit a strong primary T-cell response from the host (reviewed in references 25 and 27). Superantigens are presented to T cells by major histocompatibility complex (MHC) class II molecules on antigen-presenting cells. They differ from conventional peptide antigens by binding solely to the V␤ portion of the T-cell receptor (TCRBV) outside of the peptide-binding groove, thus forming a bridge between the T cell and the antigen-presenting cell (29). This bridging transduces a signal to the T cell, causing it to secrete cytokines that can further activate surrounding T cells. The hallmark of a superantigen response is the rapid and strong primary T-cell activation, which is MHC class II dependent and TCRBV restricted. In addition, antigen processing into peptides is not required. Both bacteria and viruses encode superantigens. The bacterial superantigens are mainly enterotoxins, which are secreted and bind externally to MHC class II molecules for presentation (34). In contrast, viral superantigens are glycosylated proteins that are endogenously produced in the infected cells.There are three families of viruses that are associated with superantigen or superantigen-like activity: Retroviridae, Rhabdoviridae, and Herpesviridae. Retroviral superantigens were first depicted in the B-type virus group in mouse mammary tumor viruses and are found in both infectious mouse mammary tumor viruses and endogenous proviruses (14,18,39,63). It has been previously shown that the env gene of HERV-K18, a defective human endogenous provirus located on chromosome 1, encodes a superantigen activity (51, 52). The HERV-K family is closely related to the B-type retroviruses based on amino acid similarity in the reverse transcriptase gene (48). HERV-K18 is a relatively recent integrant in the genome, as it is found in Old World primates but not in New World primates, indicating that it was acquired subsequent to the evolutionary divergence of these species (28). A few years ago, it was reported that Epstein-Barr virus (EBV) is associated with TCRBV13-specific superantigen activity, which is MHC class II dependent and not due to a recall antigen response (53). More recently, it was demonstrated that the superantigen activity is due to EBV transactivation of HERV-K18 env (52). We show here that this activity is dependent upon the major EBV latent gene transactivator EBNA-2, which upregulates most of the other EBV latent genes, all of which have the ability to transactivate host cell genes. In accordance with this finding, we show that the EBV latent membrane protein LMP-2A is sufficient for transactivation of HERV-K18 env.E...

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Linkage of Mls genes to endogenous mammary tumour viruses of inbred mice

Cited by 296 publications

References 35 publications

The src Homology 2 Domain-Containing Tyrosine Phosphatase 2 Regulates Primary T-Dependent Immune Responses and Th Cell Differentiation

The src Homology 2 Domain-Containing Tyrosine Phosphatase 2 Regulates Primary T-Dependent Immune Responses and Th Cell Differentiation

Factors controlling the expression of mouse mammary tumour virus

Epstein-Barr Virus Latent Membrane Protein LMP-2A Is Sufficient for Transactivation of the Human Endogenous Retrovirus HERV-K18 Superantigen

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