Dissection of tumor immune microenvironemnt in non-small cell lung cancer (NSCLC)
The tumor immune microenvironment in non–small cell lung cancer NSCLC is highly heterogeneous and plays a critical role in disease progression and response to therapy. It consists of diverse immune cell populations, such as T cells, B cells, macrophages, among others, whose functional states can promote either anti-tumor immunity or immune suppression. Understanding this complexity helps identify biomarkers and therapeutic targets, in particular for immunotherapy. One main goal is to dissect the cellular and functional immune landscape of NSCLC to improve patient stratification and optimize immunotherapeutic strategies.
Role of immunosenescence and inflammaging in healthy individuals
Immunosenescence is the age-related remodeling of the immune system, leading to reduced immune responsiveness and altered lymphocyte function. Inflammaging is a chronic, low-grade inflammatory state associated with aging. Even in healthy individuals, these processes contribute to increased infection risk, reduced vaccine responses, and susceptibility to age-related diseases. We are trying to dissect main mechanisms at the basis of these phenomena.
Immunological aging in patients affected by multiple sclerosis
Immunological aging in patients with multiple sclerosis is characterized by features of premature immunosenescence, including reduced immune repertoire diversity, accumulation of senescent and exhausted immune cells, and impaired immune regulation. These changes are accompanied by chronic inflammation, which can sustain disease activity and contribute to neurodegeneration. Together, immunosenescence and inflammaging may influence disease progression, treatment response, and long-term disability in multiple sclerosis. In this field, our main goal is to better understand the impact of immunological aging on disease mechanisms to develop targeted therapies that improve outcomes and slow progression in MS patients.
Response to vaccination and development of long-term memory
The response to vaccination and the development of long-term immune memory depend on the coordinated activation of innate and adaptive immune responses. Effective vaccines induce robust B- and T cell activation, leading to the generation of long-lived memory cells and durable antibody production. Factors such as age, immunosenescence, and chronic inflammation can impair these processes, resulting in reduced vaccine efficacy and shorter-lasting immune protection. Our main goal is to elucidate the molecular mechanisms, with a specific focus on cellular metabolism, that govern memory cell formation and maintenance.
Immunopathogenesis and response to infections by HIV and other main pathogens
The immunopathogenesis of HIV and other major viral infecations involves complex interactions between the infectious agent and the host immune system. HIV specifically targets and depletes CD4 T cells, leading to progressive immune dysfunction, chronic immune activation, and increased susceptibility to opportunistic infections. Other pathogens similarly evade or dysregulate immune responses through persistent infection, immune exhaustion, or inflammatory damage, ultimately influencing disease severity, progression, and the host’s ability to mount effective protective responses. The main goal is to uncover key immune evasion and dysregulation mechanisms in both innate and adaptive immunity in these pathological coditions.