Barbara Cassani

  • Barbara Cassani Junior Principal Investigator View More

Contact Information

  • Address
    via Manzoni 113, Building E, ground floor
  • Telephone
    +39 02 82245158
  • Fax
    +39 02 82245190
  • E-mail

Our group is interested in understanding how disruption/dysregulation of the adaptive immune system interacts with tissue microenvironment, including microbiota at barrier sites, to cause diseases such as immunodeficiency, autoimmunity and tumor. Elucidation of the underlined mechanisms is exploited to identify therapeutic targets and define novel therapy. To accomplish these goals, we combine immunological studies in patients, relevant disease and infectious models, as well as state-of-the-art high-throughput technologies. Our work has received support from the Italian Ministry of Health, the CARIPLO Foundation, the Italian Ministry of Education, Universities and Research, Telethon.

Macro-areas of research:

Role of host-microbiota interactions in the pathogenesis of primary immune deficiencies (PIDs).

Most genetic defects causing PIDs lead also to perturbations in immune surveillance at the intestinal barrier, uncovering non-redundant pathways required for intestinal colonization by critical commensals. Consistently, a substantial proportion of PID patients presents with clinically challenging IBD-like pathology. We demonstrated that dysbiosis and loss of T cell tolerance to commensals have a substantial role in determining the distinctive immune dysregulation of Omenn Syndrome, and the disease hallmark hyper-IgE.

Role of redox signalling in the regulation of intestinal homeostasis

The NADPH oxidase (NOX2) is a crucial enzyme in antimicrobial host defense and in regulating inflammation. Patients with inherited disorders of NOX2 suffer from severe life-threatening infections and excessive inflammation, including Crohn’s-like inflammatory bowel disease. In addition to phagocytes, NOX2 is also expressed by lymphocytes, though its functional implication is still poorly characterized.

Dissecting the interplay between adaptive immune responses and cellular senescence in tumorigenesis.

Hepatocellular carcinoma (HCC) is a frequent neoplasia and a leading cause of inflammation‐related cancer mortality. Despite that most HCCs arise from persistent inflammatory conditions, pathways linking chronic inflammation to cancer development are still incompletely elucidated. We recently demonstrated that adaptive immunity sustains liver fibrosis and favors HCC growth in chronic injury, by modulating innate components of inflammation and limiting the extent of hepatic stellate cells’ cellular senescence.

    Selected Publications

  • Barbara Cassani Publications

    Selected Publications: 20-25 publications listed in details with all the contributing authors, title of the papers, journal, dates. Menale C, Robinson LJ, Palagano E, Rigoni R, Erreni M, Almarza AJ, ...

Group Members