Interleukin- (IL-) 33 is an exceptional cytokine of the IL-1 family released upon tissue damage which exerts multiple functions in adaptive and innate immunity. While the cytokine has primarily been associated to atopic diseases, IL-33 has now been proven to induce cytotoxic and TH1, TH17 and regulatory T cell (Treg) functions reaching far beyond TH2 immunity. In the autoimmune disorder multiple sclerosis (MS), IL-33 is reportedly released from necrotic plaques of the central nervous system (CNS) caused by infiltrated autoreactive CD8+ T cells. In this context, it was considered fundamental to first clarify if IL-33 is systemically or rather locally active, as local, but not systemic IL-33, might modulate the activity of the autoreactive CD8+ T cells. Moreover, conditions and co-factors supporting the pro- and anti-inflammatory function of IL-33, as well as the contribution of IL-33 to the peripheral trafficking of CD8+ T cells were investigated in this doctoral thesis.
