TRIGR brings together clinical translational research on immune-mediated diseases and combines bedside with bench and vice versa. TRIGR now focuses on one overarching theme that links aging, immunity, cancer and chronic disease development. Aging is associated with clear changes in immune cell distribution and function, collectively termed immunosenescence. This progressive imbalance in the immune system is associated with increased susceptibility to infections and with reduced responses to vaccination and cancer development. Also, a chronic smoldering inflammatory state known as inflamm-aging is thought to underlie an increased incidence of immune-mediated diseases in the aging population. The TRIGR program is based on the premise that age is an intrinsic risk factor for the development of many chronic, immune-mediated systemic diseases and cancer. Many chronic diseases are triggered by an aberrant immune response to environmental challenges. Thus, understanding how the immune system dynamically develops along the life course of an individual is of major importance in terms of health and disease. Within the multidisciplinary environment formedby the TRIGR research teams, forces have been joined to focus on:
1) Evaluation of normal immune-aging and the identification of accelerating environmental and other factors. More specifically:
- What are the effects of aging per seon the healthy immune system?
- Can we identify common age-related molecular immune signatures?
- What is the effect of accelerating environmental factors such as chronic virus infection (e.g. CMV, VZV, HIV) and cancer on the immune signatures?
2) Understanding the development of chronic immune-mediated diseases. More specifically:
- Is it possible to identify individuals at risk for chronic disease development as a consequence of changes in the immune system?
- Which immune signatures (biomarkers) predict the development of immune-mediated diseases?
3) Identification of common molecular immune signatures in (late-onset) chronic inflammatory diseases. More specifically:
- Which immune signatures are shared in chronic inflammatory conditions?
- Can these common immune signatures be targeted for effective personalized treatment?
- Can we identify immune signatures associated with active disease and disease in remission (after effective treatment)?
- Can we define immune signatures thatprecede and/or predict a relapse?