Mechanisms and functions of IL-17 signaling in renal autoimmune diseases

Publication date: December 2018

Source: Molecular Immunology, Volume 104

Author(s): Tilman Schmidt, Jonas Luebbe, Hans-Joachim Paust, Ulf Panzer

Abstract

Immune-mediated glomerular diseases (glomerulonephritis) encompass a heterogeneous collection of diseases that cause inflammation within the glomerulus and other renal compartments with significant morbidity and mortality. In general, CD4⁺ T cells orchestrate the immune response and play a unique role in autoimmune and chronic inflammatory diseases. In particular, the characterization of a distinct, IL-17 cytokines producing CD4⁺ T cell subset named T_H17 cells has significantly advanced the current understanding of the pathogenic mechanisms of organ-specific immunity. Our group and others have shown that the recruitment of T_H17 cells to the inflamed kidney drives renal tissue injury in experimental and possibly human crescentic glomerulonephritis (GN), but much remains to be understood about the biological functions, regulation, and signaling pathways of the T_H17/IL-17 axis leading to organ damage. Here we review our current knowledge about the mechanisms and functions of IL-17 signaling in renal autoimmune diseases, with a special focus on experimental and human crescentic GN.

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