Targeting IL-17 in autoimmunity and inflammation

Arch Pharm Res. 2016 Nov;39(11):1537-1547. doi: 10.1007/s12272-016-0823-8. Epub 2016 Aug 30.

Abstract

The discovery of two distinct subsets of helper T cells, IFN-γ-producing Th1 cells and IL-4-producing Th2 cells, about three decades ago enabled us to understand the immunopathology of cell-mediated and allergic inflammatory diseases in humans. The observation that T cell-mediated experimental autoimmune diseases can be induced in mice lacking Th1 and Th2 cell responses prompted many immunologists to hypothesize that there might be additional subsets in helper T cell population which mediate autoimmunity in the absence of Th1 and Th2 cells. Consequently, multiple independent research groups identified IL-17-expressing RORγt+CD4+ T cell population as a distinct subset of helper T cells which promotes autoimmune tissue inflammation. Subsequent studies have revealed that innate immune cells, including γδ T cells, NKT cells and innate lymphoid cells, also produce type 17 cytokines and contribute to tissue inflammation. In this review, we discuss our current understanding on the biology of IL-17 and the therapeutic potential of targeting IL-17 for the treatment of immune disorders in humans.

Keywords: Anti-IL-17; Autoimmunity; IL-17; RORγt; Th17 cell.

Publication types

  • Review

MeSH terms

  • Animals
  • Antibodies, Monoclonal / administration & dosage
  • Antibodies, Monoclonal / therapeutic use*
  • Autoimmune Diseases / drug therapy*
  • Autoimmune Diseases / immunology
  • Autoimmunity* / drug effects
  • Cell Differentiation / drug effects
  • Cell Differentiation / immunology
  • Clinical Trials as Topic
  • Humans
  • Inflammation / drug therapy*
  • Inflammation / immunology
  • Interleukin-17 / antagonists & inhibitors*
  • Interleukin-17 / immunology
  • Receptors, Interleukin-17 / antagonists & inhibitors
  • Receptors, Interleukin-17 / immunology
  • Signal Transduction
  • Th17 Cells / cytology
  • Th17 Cells / immunology*

Substances

  • Antibodies, Monoclonal
  • Interleukin-17
  • Receptors, Interleukin-17