Lymphotoxin organizes contributions to host defense and metabolic illness from innate lymphoid cells

Cytokine Growth Factor Rev. 2014 Apr;25(2):227-33. doi: 10.1016/j.cytogfr.2013.12.007. Epub 2013 Dec 24.

Abstract

The lymphotoxin (LT)-pathway is a unique constituent branch of the Tumor Necrosis Superfamily (TNFSF). Use of LT is a critical mechanism by which fetal innate lymphoid cells regulate lymphoid organogenesis. Within recent years, adult innate lymphoid cells have been discovered to utilize this same pathway to regulate IL-22 and IL-23 production for host defense. Notably, genetic studies have linked polymorphisms in the genes encoding LTα to several phenotypes contributing to metabolic syndrome. The role of the LT-pathway may lay the foundation for a bridge between host immune response, microbiota, and metabolic syndrome. The contribution of the LT-pathway to innate lymphoid cell function and metabolic syndrome will be visited in this review.

Keywords: Host defense; Innate lymphoid cells; Lymphotoxin; Metabolic syndrome; Microbiota.

Publication types

  • Review

MeSH terms

  • Animals
  • B-Lymphocytes / immunology
  • Citrobacter rodentium / immunology
  • Humans
  • Immunity, Innate*
  • Interleukin-22
  • Interleukin-23 / biosynthesis
  • Interleukins / biosynthesis
  • Lymphotoxin beta Receptor / genetics*
  • Lymphotoxin-alpha / genetics
  • Lymphotoxin-alpha / immunology*
  • Lymphotoxin-beta / genetics
  • Lymphotoxin-beta / immunology*
  • Metabolic Syndrome / genetics
  • Mice
  • Microbiota / immunology
  • NF-kappa B p50 Subunit / biosynthesis
  • Polymorphism, Genetic
  • T-Lymphocytes / immunology
  • Transcription Factor RelA / biosynthesis

Substances

  • Interleukin-23
  • Interleukins
  • Lymphotoxin beta Receptor
  • Lymphotoxin-alpha
  • Lymphotoxin-beta
  • NF-kappa B p50 Subunit
  • RELA protein, human
  • Transcription Factor RelA