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Innate and adaptive immunity in experimental glomerulonephritis: a pathfinder tale.

Authors
  • Artinger, Katharina1
  • Kirsch, Alexander H1
  • Aringer, Ida1
  • Moschovaki-Filippidou, Foteini1
  • Eller, Philipp2
  • Rosenkranz, Alexander R1
  • Eller, Kathrin3
  • 1 Clinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 27, 8036, Graz, Austria. , (Austria)
  • 2 Intensive Care Unit, Department of Internal Medicine, Medical University of Graz, Graz, Austria. , (Austria)
  • 3 Clinical Division of Nephrology, Department of Internal Medicine, Medical University of Graz, Auenbruggerplatz 27, 8036, Graz, Austria. [email protected] , (Austria)
Type
Published Article
Journal
Pediatric Nephrology
Publisher
Springer-Verlag
Publication Date
Jun 01, 2017
Volume
32
Issue
6
Pages
943–947
Identifiers
DOI: 10.1007/s00467-016-3404-7
PMID: 27169420
Source
Medline
Keywords
License
Unknown

Abstract

The role of innate and adaptive immune cells in the experimental model of nephrotoxic serum nephritis (NTS) has been rigorously studied in recent years. The model is dependent on kidney-infiltrating T helper (TH) 17 and TH1 cells, which recruit neutrophils and macrophages, respectively, and cause sustained kidney inflammation. In a later phase of disease, regulatory T cells (Tregs) infiltrate the kidney in an attempt to limit disease activity. In the early stage of NTS, lymph node drainage plays an important role in disease initiation since dendritic cells present the antigen to T cells in the T cell zones of the draining lymph nodes. This results in the differentiation and proliferation of TH17 and TH1 cells. In this setting, immune regulatory cells (Tregs), namely, CCR7-expressing Tregs and mast cells (MCs), which are recruited by Tregs via the production of interleukin-9, exert their immunosuppressive capacity. Together, these two cell populations inhibit T cell differentiation and proliferation, thereby limiting disease activity by as yet unknown mechanisms. In contrast, the spleen plays no role in immune activation in NTS, but constitutes a place of extramedullary haematopoiesis. The complex interactions of immune cells in NTS are still under investigation and might ultimately lead to targeted therapies in glomerulonephritis.

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