Servizio Comunitario di Informazione in materia di Ricerca e Sviluppo - CORDIS

Final Activity Report Summary - TRIPR (Translational Research in Paediatric Rheumatology)

TRIPR was a coherent series of events that endeavoured to acquaint younger generations of European researchers and clinicians with the key issues underlying the development of new therapeutic strategies for paediatric rheumatic diseases, seeking above all to expose them to emerging methodologies driving novel translational strategies and approaches in the field. Parallel to this overriding aim was the intent to enhance the European contribution to:
a) the understanding of pathogenic mechanisms in rheumatic disorders;
b) the discovery of new therapeutic approaches;
c) the definition of the best models for rare conditions such as childhood rheumatic diseases to test new potential effective drugs/agents.

Lastly, the series events was intentionally conceived to appeal also to adult rheumatologists, with the aim to foster relations and lead to the creation of an even more extensive network among European researchers interested in chronic inflammation.

The leadoff conference, "Anticipating changes in drug development for Children: Building on Paediatric Rheumatology" (May 29th - June 1st, 2008, Genoa, Italy), focused on the methodologies to facilitate and implement clinical trials in children with rare disorders and on the pertinent related regulatory issues. Using the field of rare paediatric rheumatic disorders as a paradigm, the event examined the medicinal research and development process, from pre-clinical and early-phase clinical development, to biomarker validation, study design and management, data analysis, ethical review, regulatory submission and research governance.

The second event "Innate Immunity and the Pathogenesis of Rheumatic Diseases" (May 6-9, 2009; Genoa, Italy), showcased the study of pathogen-associated molecular patterns (PAMPs)- and damage associated molecular pattern molecules (DAMPs)-mediated innate immunity activation as a very promising frontier in research related to the pathogenesis of chronic rheumatic diseases, and one which could ultimately lead to the identification of drugs that can selectively target and/or modulate the activity of the innate immune system.

The third conference "Adaptive Immunity and the Pathogenesis of Rheumatic Diseases" (September 24-27, 2009; Genoa, Italy) focused on the molecular and cellular mechanisms involved in the activation of the effector functions of the adaptive immune system, their involvement in the pathogenesis of chronic rheumatic diseases and the identification of targets to modulate the activity of the adaptive immune system, exploring above all:
1) the pivotal role of central and peripheral B and T cell development in the pathogenesis of autoimmune diseases;
2) the role of B lymphocytes not only as precursors of autoantibody secreting cells, but also as regulators of autoreactive T cell responses;
3) breakthroughs in the understanding of regulatory T cells, of new mechanisms governing immune tolerance, and of T helper 17 (Th17) cells.

Each of these fields has generated profound insight into inflammatory and autoimmune diseases and has opened new potential avenues for the treatment of rheumatic disorders. Building also on the outcome of the first 3 conferences, the fourth and final event "Biological Agents and Emerging Treatments in the Management of Rheumatic Diseases" (May 27-30, 2010) addressed the treatment of both adult and childhood rheumatic diseases with the purpose of reviewing and discussing the progress that has been achieved thus far, the unmet needs that are still faced, and the potential new treatments that the future holds in store.

To close the cycle on bringing discoveries to fruition, a final session examined strategies to improve methodologies of translational research on and clinical development in common, as well as rare, forms of rheumatic disorders. Overall, the four conferences attracted a total of 340 attendees, of whom 179 were eligible event participants, 61 fewer than estimated.

Reported by