Interplay of innate lymphoid cells and regulatory T cells in NLRP3 inflammasome-dependent nephritis

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Inflammasome-induced nephritis is mainly triggered by activated dendritic cells and macrophages via the production of pro-inflammatory cytokines such as IL-1b, TNF, IL-6 and IL-18. Preliminary experiments suggest a connection between inflammation on the composition of innate lymphoid cells in the kidney. ILC seem to promote an inflamed environment by enhancing the inflammatory process and by interacting with CD4+ T helper cells. The composition of cytokines suggested a permissive environment for Th17 lymphocytes during kidney inflammation, but it may also induce innate lymphoid cells especially of subpopulation 3. This project will investigate the interplay of regulatory T cells and ILC in NLRP3-inflammasome-induced kidney inflammation. Here, we will specifically focus on the role of NLRP3-inflammasome-induced cytokines on the activation and plasticity of the renal ILC populations. In particular, we will investigate the local and systemic effects of inflammation and inflammatory cytokines on the function and composition renal and splenic ILCs. Furthermore, the suppressive or modulating capacity of Tregs and the underlying mechanism of Tregs on renal ILCs will be elucidated.