Search

The ATHENA X-ray telescope will be the largest X-ray optics ever built. The ground calibration of this mirror assembly raises significant difficulties due to its unprecedented size, mass and focal length. The VERT-X project aims at developing an innovative calibration system which will be able to accomplish to this extremely challenging task.The design is based on an X-ray parallel beam produced by an X-ray source positioned in the focus of a highly performing X-ray collimator; the beam will be accurately moved by a raster-scan mechanism covering all the ATHENA optics at different off-axis angles. The main driving factor in the VERT-X design is the ATHENA calibration requirement on the accuracy in the HEW measure which is 0.1”, all over the field of view. The VERT-X project, started in January 2019, is financed by ESA and conducted by a consortium that includes INAF together with EIE, Media Lario, BCV Progetti and GPAP.

We investigated the role of chemokines in regulating T cell accumulation in solid tumors. CCL5 and CXCL9 overexpression was associated with CD8+ T cell infiltration in solid tumors. T cell infiltration required tumor cell-derived CCL5 and was amplified by IFN-γ-inducible, myeloid cell-secreted CXCL9. CCL5 and CXCL9 coexpression revealed immunoreactive tumors with prolonged survival and response to checkpoint blockade. Loss of CCL5 expression in human tumors was associated with epigenetic silencing through DNA methylation. Reduction of CCL5 expression caused tumor-infiltrating lymphocyte (TIL) desertification, whereas forced CCL5 expression prevented Cxcl9 expression and TILs loss, and attenuated tumor growth in mice through IFN-γ. The cooperation between tumor-derived CCL5 and IFN-γ-inducible CXCR3 ligands secreted by myeloid cells is key for orchestrating T cell infiltration in immunoreactive and immunoresponsive tumors. Dangaj et al. show that tumor cell-expressed CCL5 and macrophage- and DC-expressed CXCL9 are important for the infiltration of T cells into tumors, a process that also requires recognition of tumor antigens by T cells. CCL5 is often epigenetically silenced in tumor cells but can be reactivated by Decitabine. © 2019 Elsevier Inc.