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Anja Schmidt-Christensen

Assistant researcher

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NKT cells promote both type 1 and type 2 inflammatory responses in a mouse model of liver fibrosis

Author

  • Julia Nilsson
  • Maria Hörnberg
  • Anja Schmidt-Christensen
  • Kajsa Linde
  • Maria Nilsson
  • Marine Carlus
  • Saskia F. Erttmann
  • Sofia Mayans
  • Dan Holmberg

Summary, in English

Sterile liver inflammation and fibrosis are associated with many liver disorders of different etiologies. Both type 1 and type 2 inflammatory responses have been reported to contribute to liver pathology. However, the mechanisms controlling the balance between these responses are largely unknown. Natural killer T (NKT) cells can be activated to rapidly secrete cytokines and chemokines associated with both type 1 and type 2 inflammatory responses. As these proteins have been reported to accumulate in different types of sterile liver inflammation, we hypothesized that these cells may play a role in this pathological process. We have found that a transgenic NKT (tgNKT) cell population produced in the immunodeficient 2,4αβNOD.Rag2−/− mice, but not in 2,4αβNOD.Rag2+/− control mice, promoted a type 1 inflammatory response with engagement of the NOD-, LRR- and pyrin domain-containing protein-3 (NLRP3) inflammasome. The induction of the type 1 inflammatory response was followed by an altered cytokine profile of the tgNKT cell population with a biased production of anti-inflammatory/profibrotic cytokines and development of liver fibrosis. These findings illustrate how the plasticity of NKT cells modulates the inflammatory response, suggesting a key role for the NKT cell population in the control of sterile liver inflammation.

Department/s

  • Autoimmunity
  • EXODIAB: Excellence of Diabetes Research in Sweden

Publishing year

2020

Language

English

Publication/Series

Scientific Reports

Volume

10

Issue

1

Document type

Journal article

Publisher

Nature Publishing Group

Topic

  • Immunology in the medical area

Status

Published

Research group

  • Autoimmunity

ISBN/ISSN/Other

  • ISSN: 2045-2322