Regulatory T cells and type 2 innate lymphoid cell-dependent asthma

Allergy. 2017 Aug;72(8):1148-1155. doi: 10.1111/all.13139. Epub 2017 Mar 1.

Abstract

Group 2 innate lymphoid cells (ILC2s) are a recently identified group of cells with the potent capability to produce Th2-type cytokines such as interleukin (IL)-5 and IL-13. Several studies suggest that ILC2s play an important role in the development of allergic diseases and asthma. Activation of pulmonary ILC2s in murine models lacking T and B cells induces eosinophilia and airway hyper-reactivity (AHR), which are cardinal features of asthma. More importantly, numerous recent studies have highlighted the role of ILC2s in asthma persistence and exacerbation among human subjects, and thus, regulation of pulmonary ILC2s is a major area of investigation aimed at curbing allergic lung inflammation and exacerbation. Emerging evidence reveals that a group of regulatory T cells, induced Tregs (iTregs), effectively suppress the production of ILC2-driven, pro-inflammatory cytokines IL-5 and IL-13. The inhibitory effects of iTregs are blocked by preventing direct cellular contact or by inhibiting the ICOS-ICOS-ligand (ICOSL) pathway, suggesting that both direct contact and ICOS-ICOSL interaction are important in the regulation of ILC2 function. Also, cytokines such as IL-10 and TGF-β1 significantly reduce cytokine secretion by ILC2s. Altogether, these new findings uncover iTregs as potent regulators of ILC2 activation and implicate their utility as a therapeutic approach for the treatment of ILC2-mediated allergic asthma and respiratory disease.

Keywords: ICOS; Treg; asthma; innate lymphoid cells; regulatory aspects.

Publication types

  • Review

MeSH terms

  • Animals
  • Asthma / immunology*
  • Asthma / metabolism
  • Biomarkers
  • Cell Separation
  • Cytokines / metabolism
  • Disease Models, Animal
  • Humans
  • Immunity, Innate*
  • Immunomodulation
  • Immunophenotyping
  • Inducible T-Cell Co-Stimulator Ligand / metabolism
  • Inducible T-Cell Co-Stimulator Protein / metabolism
  • Inflammation Mediators / metabolism
  • Protein Binding
  • Respiratory Hypersensitivity / immunology
  • Respiratory Hypersensitivity / metabolism
  • T-Lymphocyte Subsets / immunology*
  • T-Lymphocyte Subsets / metabolism
  • T-Lymphocytes, Regulatory / immunology*
  • T-Lymphocytes, Regulatory / metabolism
  • Th2 Cells / immunology*
  • Th2 Cells / metabolism
  • Translational Research, Biomedical

Substances

  • Biomarkers
  • Cytokines
  • Inducible T-Cell Co-Stimulator Ligand
  • Inducible T-Cell Co-Stimulator Protein
  • Inflammation Mediators