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Innate lymphoid cells in renal inflammation


In the last few years a new population of lymphocytes that belongs to the innate arm of the immune system has been identified and studied extensively. Because of their antigen-independent activation and lymphoid morphology these cells have been termed “Innate Lymphoid Cells“ (ILCs).

In recent studies by us and others, it has been shown that IL-5- and IL-13-producing ILCs are crucial for the regulation of eosinophil abundance and the differentiation of alternatively activated macrophages in various tissues. Thereby, and by producing mediators that directly enhance epithelial regeneration, these ILCs can contribute to tissue remodeling and repair processes after acute tissue injury.

First evidence indicates that ILCs are present in the healthy human and murine kidney and that the sustained expansion of kidney-residing ILCs by systemic cytokine treatment can enhance tissue repair in mouse models of kidney injury. The role of ILC subtypes in the kidney as a source of T helper-cell-associated cytokines and their function in renal inflammation await further study.

The long-term aim of the Emmy Noether Research Group, funded by the DFG since March 2015, will be to evaluate kidney-residing ILCs as a potential therapeutic target for modulation of the immune response in inflammatory kidney diseases.


Function IL-22 and IL-9 in glomerulonephritis (part of the SFB 1192)


The cytokines IL-22 and IL-9 are important regulators of tissue responses in inflammation and under homeostatic conditions. They are produced by T cell subsets and cells of the innate immune system, including ILCs. While IL-22 signaling exclusively targets tissue resident cells, IL-9 mainly exerts its effect by modulating the function of immune cells in an auto- and paracrine manner. Both cytokines have been implicated in autoimmune inflammation, as well as in tissue remodeling and repair processes. The role of these mediators in kidney disease is largely unknown.

As a part of the Collaborative Research Centre 1192 “Immune-mediated glomerular disease” this project investigates the function of IL-22- and IL-9-producing immune cells in the immunopathogenesis of glomerulonephritis (GN) by using mouse models for GN and patient samples. The long-term aim is to increase the understanding of IL-22 and IL-9 biology in renal inflammation and to potentially identify novel therapeutic targets for treatment of patients with immune-mediated glomerular diseases.

Selected Publications

Düster M, Becker M, Gnirck AC, Wunderlich M, Panzer U, Turner JE (2018): T cell-derived IFN-γ downregulates protective group 2 innate lymphoid cells in murine lupus erythematosus. Eur J Immunol 2018 Apr 19. [Epub ahead of print]

Xiong T, Turner JE (2018): Innate lymphoid cells in autoimmunity and chronic inflammatory diseases. Semin Immunopathol 2018 Mar 22. [epub ahead of print]

Turner JE, Becker M, Mittrücker HW, Panzer U (2018): Tissue-Resident Lymphocytes in the Kidney. J Am Soc Nephrol 29:389-399.

Riedel JH, Becker M, Kopp K, Duster M, Brix SR, Meyer-Schwesinger C, Kluth LA, Gnirck AC, Attar M, Krohn S, Fehse B, Stahl RA, Panzer U, Turner JE (2017): IL-33-Mediated Expansion of Type 2 Innate Lymphoid Cells Protects from Progressive Glomerulosclerosis. J Am Soc Nephrol [epub ahead of print]

Krebs CF, Paust HJ, Krohn S, Koyro T, Brix SR, Riedel JH, Bartsch P, Wiech T, Meyer-Schwesinger C, Huang J, Fischer N, Busch P, Mittrucker HW, Steinhoff U, Stockinger B, Perez LG, Wenzel UO, Janneck M, Steinmetz OM, Gagliani N, Stahl RA, Huber S, Turner JE, Panzer U (2016): Autoimmune Renal Disease Is Exacerbated by S1P-Receptor-1-Dependent Intestinal Th17 Cell Migration to the Kidney. Immunity 45:1078-92

Turner JE, Morrison PJ, Wilhelm C, Wilson M, Ahlfors H, Renauld JC, Panzer U, Helmby H, Stockinger B (2013). IL-9-mediated survival of type 2 innate lymphoid cells promotes damage control in helminth-induced lung inflammation. J Exp Med 210:2951-65

Turner JE, Stockinger B, Helmby H (2013). IL-22 Mediates Goblet Cell Hyperplasia and Worm Expulsion in Intestinal Helminth Infection. PLoS Pathog 9:e1003698

Hirota K, Turner JE, Villa M, Duarte JH, Demengeot J, Steinmetz OM, Stockinger B (2013). Plasticity of TH17 cells in Peyer's patches is responsible for the induction of T cell-dependent IgA responses. Nat Immunol 14:372-9

Wilhelm C, Turner JE, Van Snick J, Stockinger B (2012). The many lives of IL-9: a question of survival? Nat Immunol 13:637-41

Turner JE, Krebs C, Tittel AP, Paust HJ, Meyer-Schwesinger C, Bennstein SB, Steinmetz OM, Prinz I, Magnus T, Korn T, Stahl RA, Kurts C, Panzer U (2012). IL-17A production by renal gammadelta T cells promotes kidney injury in crescentic GN. J Am Soc Nephrol 23:1486-95