Giovanna Schiavoni

ICSBP is essential for the development of mouse type I interferon-producing cells and for the generation and activation of CD8alpha(+) dendritic cells.

ICSBP is critically involved in the normal development and trafficking of Langerhans cells and dermal dendritic cells.

Type I IFN protects permissive macrophages from Legionella pneumophila infection through an IFN-gamma-independent pathway.

ICSBP/IRF-8 differentially regulates antigen uptake during dendritic-cell development and affects antigen presentation to CD4+ T cells.

Type I IFN regulate DC turnover in vivo.

Cyclophosphamide synergizes with type I interferons through systemic dendritic cell reactivation and induction of immunogenic tumor apoptosis.

Type I IFNs control antigen retention and survival of CD8α(+) dendritic cells after uptake of tumor apoptotic cells leading to cross-priming.

IRF-8 controls melanoma progression by regulating the cross talk between cancer and immune cells within the tumor microenvironment.

TIM-3 as a molecular switch for tumor escape from innate immunity.

Novel allergic asthma model demonstrates ST2-dependent dendritic cell targeting by cypress pollen.

The tumor microenvironment: a pitch for multiple players.

Interferon regulatory factor 8-deficiency determines massive neutrophil recruitment but T cell defect in fast growing granulomas during tuberculosis.

Mycobacterium tuberculosis PstS1 amplifies IFN-γ and induces IL-17/IL-22 responses by unrelated memory CD4+ T cells via dendritic cell activation.

The dual role of IRF8 in cancer immunosurveillance.

Type I Interferons as Stimulators of DC-Mediated Cross-Priming: Impact on Anti-Tumor Response.

Cancer-driven dynamics of immune cells in a microfluidic environment.

Chemotherapy-induced antitumor immunity requires formyl peptide receptor 1.

Chemo-immunotherapy induces tumor regression in a mouse model of spontaneous mammary carcinogenesis.

Combining Type I Interferons and 5-Aza-2'-Deoxycitidine to improve anti-tumor response against melanoma.

The dangerous liaison between pollens and pollution in respiratory allergy.

IL-33 restricts tumor growth and inhibits pulmonary metastasis in melanoma-bearing mice through eosinophils.

Organs on chip approach: a tool to evaluate cancer -immune cells interactions.

Eosinophils: The unsung heroes in cancer?

Disruption of IFN-I Signaling Promotes HER2/Neu Tumor Progression and Breast Cancer Stem Cells.

The Pleiotropic Immunomodulatory Functions of IL-33 and Its Implications in Tumor Immunity.

From Petri Dishes to Organ on Chip Platform: The Increasing Importance of Machine Learning and Image Analysis.

IL-33 Promotes CD11b/CD18-Mediated Adhesion of Eosinophils to Cancer Cells and Synapse-Polarized Degranulation Leading to Tumor Cell Killing.

High-throughput analysis of cell-cell crosstalk in ad hoc designed microfluidic chips for oncoimmunology applications.

Basophils in Tumor Microenvironment and Surroundings.

Tumor-Intrinsic or Drug-Induced Immunogenicity Dictates the Therapeutic Success of the PD1/PDL Axis Blockade.

Multicentre Harmonisation of a Six-Colour Flow Cytometry Panel for Naïve/Memory T Cell Immunomonitoring.

Corrigendum to "Multicentre Harmonisation of a Six-Colour Flow Cytometry Panel for Naïve/Memory T Cell Immunomonitoring".

Is There a Role for Basophils in Cancer?

Eosinophils in the Tumor Microenvironment.

Anti-Tumorigenic Activities of IL-33: A Mechanistic Insight.

A Clonogenic Assay to Quantify Melanoma Micrometastases in Pulmonary Tissue.

Oncoimmunology Meets Organs-on-Chip.