4 research outputs found

    Nonlinear realisation approach to topologically massive supergravity

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    We develop a nonlinear realisation approach to topologically massive supergravity in three dimensions, with and without a cosmological term. It is a natural generalisation of a similar construction for N=1{\cal N}=1 supergravity in four dimensions, which was recently proposed by one of us. At the heart of both formulations is the nonlinear realisation approach to gravity which was given by Volkov and Soroka fifty years ago in the context of spontaneously broken local supersymmetry. In our setting, the action for cosmological topologically massive supergravity is invariant under two different local supersymmetries. One of them acts on the Goldstino, while the other supersymmetry leaves the Goldstino invariant. The former can be used to gauge away the Goldstino, and then the resulting action coincides with that given in the literature.Comment: 29 page

    New duality-invariant models for nonlinear supersymmetric electrodynamics

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    We propose a new family of U(1)\mathsf{U}(1) duality-invariant models for nonlinear N=1{\cal N}=1 supersymmetric electrodynamics coupled to supergravity. This family includes the Cribiori-Farakos-Tournoy-van Proeyen supergravity-matter theory for spontaneously broken local supersymmetry with a novel Fayet-Iliopoulos term without gauged RR-symmetry. We present superconformal duality-invariant models.Comment: 15 page

    New duality-invariant models for nonlinear supersymmetric electrodynamics

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    Abstract We propose a new family of U(1) duality-invariant models for nonlinear N N \mathcal{N} = 1 supersymmetric electrodynamics coupled to supergravity. It includes the Cribiori-Farakos-Tournoy-van Proeyen supergravity-matter theory for spontaneously broken local supersymmetry with a novel Fayet-Iliopoulos term without gauged R-symmetry. We present superconformal duality-invariant models, as well as new U(1) duality-invariant models for spontaneously broken local supersymmetry

    The anti-cancer agents lenalidomide and pomalidomide inhibit the proliferation and function of T regulatory cells

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    Lenalidomide (Revlimid®; CC-5013) and pomalidomide (CC-4047) are IMiDs® proprietary drugs having immunomodulatory properties that have both shown activity in cancer clinical trials; lenalidomide is approved in the United States for a subset of MDS patients and for treatment of patients with multiple myeloma when used in combination with dexamethasone. These drugs exhibit a range of interesting clinical properties, including anti-angiogenic, anti-proliferative, and pro-erythropoietic activities although exact cellular target(s) remain unclear. Also, anti-inflammatory effects on LPS-stimulated monocytes (TNF-α is decreased) and costimulatory effects on anti-CD3 stimulated T cells, (enhanced T cell proliferation and proinflammatory cytokine production) are observed These drugs also cause augmentation of NK-cell cytotoxic activity against tumour-cell targets. Having shown that pomalidomide confers T cell-dependant adjuvant-like protection in a preclinical whole tumour-cell vaccine-model, we now show that lenalidomide and pomalidomide strongly inhibit T-regulatory cell proliferation and suppressor-function. Both drugs inhibit IL-2-mediated generation of FOXP3 positive CTLA-4 positive CD25high CD4+ T regulatory cells from PBMCs by upto 50%. Furthermore, suppressor function of pre-treated T regulatory cells against autologous responder-cells is abolished or markedly inhibited without drug related cytotoxicity. Also, Balb/C mice exhibit 25% reduction of lymph-node T regulatory cells after pomalidomide treatment. Inhibition of T regulatory cell function was not due to changes in TGF-β or IL-10 production but was associated with decreased T regulatory cell FOXP3 expression. In conclusion, our data provide one explanation for adjuvant properties of lenalidomide and pomalidomide and suggest that they may help overcome an important barrier to tumour-specific immunity in cancer patients
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