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Vettorazzi, S.

Publications and source records attributed to Vettorazzi, S..

2 recordsLinked to original sources

Multi-omic and spatial analysis reveals tumour-derived paracrine signals drive suppressive macrophage polarisation via activation of the cAMP-CREB axis in glioblastoma

Tumor-associated macrophages (TAMs) are key mediators of tumor immunosuppression, yet the factors governing their polarization remain poorly understood, especially in highly immunosuppressive cancers, including cancers affecting the central nervous system. This study investigates the molecular pathways underlying TAM polarization in glioblastoma, one of the most immunosuppressive cancer types. Using a multi-omics approach integrating spatial proteomics, RNA-sequencing, and proteomic profiling of tumor cells and macrophages, we demonstrate that circulating monocytes polarize toward an immunosuppressive state when they exit tumor blood vessels, in response to glioblastoma cell-secreted cytokines. In situ and in vitro data shows that macrophage polarization is regulated via the cAMP-CREB signaling-transcription axis.

cancer biology↗

IgD-Expressing Mature B Cells Exhibit Enhanced Sensitivity to Glucocorticoid-Induced Cell Death

Glucocorticoids (GCs) regulate diverse physiological processes, comprising metabolism, immune responses, stress adaptation and inflammation. Synthetic GCs are widely used for their powerful anti-inflammatory and immunosuppressive effects, in the treatment of autoimmune diseases, allergies, and inflammation. Here, we investigated the role of the glucocorticoid receptor (GR) in B cell development and survival using both B cell-specific GR-deficient mice and continuous in vivo GR agonist treatments. Deletion of the GR in B cells altered splenic B cell subpopulations, increasing follicular and CD21lo B cells and leading to the accumulation of IgM-/IgD- B cells. In vivo treatment with GR agonists, such as Dexamethasone (Dex) and Prednisolone (Pred), selectively depleted IgDhigh follicular B cells while enriching IgDlow marginal zone B cells. IgDlow (IgMhigh) B cells, which were more resistant to glucocorticoid-induced cell death, showed increased expression of IL-10 and genes involved in survival, suggesting a potential regulatory function. In vitro, B cell activation via CpG or LPS altered IgM/IgD expression and B cell sensitivity to GR agonists, thereby leading to improved B cell survival and increased plasma cell differentiation. Together, these findings suggest that IgD downregulation and IgM upregulation are critical for B cell survival under GC exposure and that GR agonists promote the enrichment of IgDlow (IgMhigh) cells resistant to apoptosis.

immunology↗