---

Secondary lymphoid tissues (SLTs) are an absolute requirement for lymphocyte activation. Alymphoplastic (NIK-aly/aly) mice lack lymph nodes and display impaired immunity. The malformations of NIK-aly/aly mice are due to a mutation in the NFkB-inducing kinase (NIK). NIK is involved in the formation of SLTs during development. To our surprise, we found that the immunodeficiency of NIK-aly/aly mice results from the impact of NIK on T cell priming but not from the lack of SLTs. We describe an alternative pathway for the induction of cell-mediated immunity, in which antigen-presenting cells sample antigen and migrate into the liver where they induce neo-lymphoid aggregates. We further demonstrate that the NIK-lesion in NIK-aly/aly mice does not cause an intrinsic T cell defect but leads to the failure of dendritic cells to licence CD4+ effector lineages. In detail we discovered that a population of thymic DCs requires NIK and is capable to shape the formation of T effector lineages during thymic T cell development.

---

studied Biology at the Johann-Wolfgang Goethe University of Frankfurt (M). She completed her diploma thesis in the Immunology devision of the Federal Institute of Sera and Vaccines in Langen, before she went for her doctoral studies to the University of Zurich, which she completed under the supervision of Prof. Burkhard Becher in 2011.

---