Novel effector molecules in type 2 inflammation: lessons drawn from helminth infection and allergy

J Immunol. 2006 Aug 1;177(3):1393-9. doi: 10.4049/jimmunol.177.3.1393.

Abstract

Type 2 cytokine-induced inflammatory responses are critical components of the mucosal immune response required for host defense against helminth infection and are also responsible for the pathogenesis of many debilitating diseases including asthma, allergy, and forms of inflammatory bowel disease. Given the global prevalence of helminth infections, with an estimated two billion individuals infected worldwide, and the pandemic levels of asthma and allergy, with 30% of the population affected in North America, it is essential to define the molecules and pathways that underlie the protective or pathologic consequences of type 2 inflammation. In this review, we will focus on four families of proteins that are highly induced in helminth infection and allergy: 1) the arginases; 2) the resistin-like molecules; 3) the chitinase-like mammalian proteins; and 4) the intelectins. Here, we summarize what is known about their regulation and potential function in protecting against infection and/or exacerbating inflammation.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Amino Acid Sequence
  • Animals
  • Cytokines / biosynthesis*
  • Cytokines / classification*
  • Cytokines / genetics
  • Cytokines / physiology
  • Helminthiasis, Animal / enzymology
  • Helminthiasis, Animal / immunology*
  • Helminthiasis, Animal / pathology*
  • Helminthiasis, Animal / prevention & control
  • Humans
  • Hypersensitivity / enzymology
  • Hypersensitivity / immunology*
  • Hypersensitivity / pathology*
  • Hypersensitivity / prevention & control
  • Inflammation Mediators / classification*
  • Inflammation Mediators / metabolism
  • Inflammation Mediators / physiology*
  • Molecular Sequence Data

Substances

  • Cytokines
  • Inflammation Mediators