Exploring novel correlations in trilepton channels at the LHC for the minimal supersymmetric inverse seesaw model

We investigate signatures of the minimal supersymmetric inverse seesaw model at the large hadron collider (LHC) with three isolated leptons and large missing energy (3\ell + \mET or 2\ell + 1\tau + \mET, with \ell=e,\mu) in the final state. This signal has its origin in the decay of chargino-neutralino (\chpm1\ntrl2) pair, produced in pp collisions. The two body decays of the lighter chargino into a charged lepton and a singlet sneutrino has a characteristic decay pattern which is correlated with the observed large atmospheric neutrino mixing angle. This correlation is potentially observable at the LHC by looking at the ratios of cross sections of the trilepton + \mET channels in certain flavour specific modes. We show that even after considering possible leading standard model backgrounds these final states can lead to reasonable discovery significance at the LHC with both 7 TeV and 14 TeV center-of-mass energy.Comment: 28 pages, 9 .eps figures. 3 new figures and discussions on LHC observables added, minor modifications in text and in the abstract, 23 new references added, matches with the published version in JHE

Parasite fate and involvement of infected cells in the induction of CD4+ and CD8+ T cell responses to Toxoplasma gondii

During infection with the intracellular parasite Toxoplasma gondii, the presentation of parasite-derived antigens to CD4+ and CD8+ T cells is essential for long-term resistance to this pathogen. Fundamental questions remain regarding the roles of phagocytosis and active invasion in the events that lead to the processing and presentation of parasite antigens. To understand the most proximal events in this process, an attenuated non-replicating strain of T. gondii (the cpsII strain) was combined with a cytometry-based approach to distinguish active invasion from phagocytic uptake. In vivo studies revealed that T. gondii disproportionately infected dendritic cells and macrophages, and that infected dendritic cells and macrophages displayed an activated phenotype characterized by enhanced levels of CD86 compared to cells that had phagocytosed the parasite, thus suggesting a role for these cells in priming naïve T cells. Indeed, dendritic cells were required for optimal CD4+ and CD8+ T cell responses, and the phagocytosis of heat-killed or invasion-blocked parasites was not sufficient to induce T cell responses. Rather, the selective transfer of cpsII-infected dendritic cells or macrophages (but not those that had phagocytosed the parasite) to naïve mice potently induced CD4+ and CD8+ T cell responses, and conferred protection against challenge with virulent T. gondii. Collectively, these results point toward a critical role for actively infected host cells in initiating T. gondii-specific CD4+ and CD8+ T cell responses

Biomarkers, genetic association, and genomic studies

Rheumatoid arthritis (RA) is a common autoimmune disorder which shows clinical heterogeneity. IT has multiple treatment options and there is individual variation in response to treatment. These features make RA an ideal condition to develop biomarkers for its pre-clinical detection, diagnosis, subtyping, prognostic stratification and selection of most optimal treatment. While a number of markers have been assessed for their biomarker quality, currently no marker has the statistical properties of a biomarker to be considered as a good classifier. In this chapter, a general review of biomarkers is followed by a detailed discussion of biomarker candidates for various aspects of RA. It is unlikely that a single marker will ever be sufficiently powerful as a biomarker, but combinations of clinical, biochemical, genetic, epigenetic, proteomic and metabolomic markers have the strongest potential to fulfill the requirements of biomarkers. Given the high heritability of RA and the progress in methodology of genome-wide association studies, genetic markers are the most promising group to be developed as biomarkers, in particular when epigenetic markers become more widely used. It is possible that in the near future, biomarkers with documented clinical utility will be available for use in clinical decision making and will most probably use multiple omics platforms