Making research relevant to policy-makers, development actors, and local communities: NCCR North-South report on effectiveness of research for development

Bridging the gap between research and policy is of growing importance in international development. The National Centre of Competence in Research (NCCR) North-South has rich experience in collaborating beyond academic boundaries to make their research relevant to various societal actors. This publication is the first to provide an overview of the effectiveness of NCCR North-South researchers’ efforts to interact with policy, practice, and local communities with a view to effecting a change in practices. A systematic assessment of researchers’ interactions with non-academic partners is presented, based on principles of monitoring and evaluation. On this basis, tools for collective learning and widespread adaptation are proposed. The report shows with what types of societal actors NCCR North-South researchers collaborate and analyses examples of how researchers conduct dialogue beyond academic boundaries, leading to specific outcomes. It also explains the frame conditions considered decisive for successful and sustainable policy dialogue and concludes with recommendations about how the NCCR North-South can increase the effectiveness of its research for development. The publication is a valuable source of inspiration for those interested in better understanding how to generate the multiple benefits of making science relevant to society.

Overexpression of lymphotoxin in T cells induces fulminant thymic involution

Activated lymphocytes and lymphoid-tissue inducer cells express lymphotoxins (LTs), which are essential for the organogenesis and maintenance of lymphoreticular microenvironments. Here we describe that T-cell-restricted overexpression of LT induces fulminant thymic involution. This phenotype was prevented by ablation of the LT receptors tumor necrosis factor receptor (TNFR) 1 or LT beta receptor (LTbetaR), representing two non-redundant pathways. Multiple lines of transgenic Ltalphabeta and Ltalpha mice show such a phenotype, which was not observed on overexpression of LTbeta alone. Reciprocal bone marrow transfers between LT-overexpressing and receptor-ablated mice show that involution was not due to a T cell-autonomous defect but was triggered by TNFR1 and LTbetaR signaling to radioresistant stromal cells. Thymic involution was partially prevented by the removal of one allele of LTbetaR but not of TNFR1, establishing a hierarchy in these signaling events. Infection with the lymphocytic choriomeningitis virus triggered a similar thymic pathology in wt, but not in Tnfr1(-/-) mice. These mice displayed elevated TNFalpha in both thymus and plasma, as well as increased LTs on both CD8(+) and CD4(-)CD8(-) thymocytes. These findings suggest that enhanced T cell-derived LT expression helps to control the physiological size of the thymic stroma and accelerates its involution via TNFR1/LTbetaR signaling in pathological conditions and possibly also in normal aging.