Who Chooses? Which Hartford students are likely to apply to a different public school operated by the City?

Hartford has the lowest student achievement test scores in the State of Connecticut, which is also the state with the highest achievement gap. Since 2008 Hartford students have had the choice to apply to a variety of schools, including Hartford public neighborhood schools, Hartford public interdistrict magnet schools, and suburban Open Choice schools. The rationale for open choice is primarily to allow parents to choose better performing schools, driving out the lower performing schools, thus improving the achievement level of Hartford students. In our research we attempt to answer: “Which Hartford students were more likely to exercise choice?” We use data on all Hartford Public School students grades 3-8. We expect to find students making applications to higher performing schools. We found, however, that very few students who are currently attending a HPS apply to another HP neighborhood school. Of these applications, 30% was to Achievement First, the only HP district school with a high achievement score. Movement to this high performing school was almost exclusively from the north end, where the school is located. Virtually no applications came from the south end of Hartford

CIS is a potent checkpoint in NK cell-mediated tumor immunity

The detection of aberrant cells by natural killer (NK) cells is controlled by the integration of signals from activating and inhibitory ligands and from cytokines such as IL-15. We identified cytokine-inducible SH2-containing protein (CIS, encoded by Cish) as a critical negative regulator of IL-15 signaling in NK cells. Cish was rapidly induced in response to IL-15, and deletion of Cish rendered NK cells hypersensitive to IL-15, as evidenced by enhanced proliferation, survival, IFN-γ production and cytotoxicity toward tumors. This was associated with increased JAK-STAT signaling in NK cells in which Cish was deleted. Correspondingly, CIS interacted with the tyrosine kinase JAK1, inhibiting its enzymatic activity and targeting JAK for proteasomal degradation. Cish -/- mice were resistant to melanoma, prostate and breast cancer metastasis in vivo, and this was intrinsic to NK cell activity. Our data uncover a potent intracellular checkpoint in NK cell-mediated tumor immunity and suggest possibilities for new cancer immunotherapies directed at blocking CIS function