A human homologue of the Drosophila Toll protein signals activation of adaptive immunity View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

1997-07

AUTHORS

R Medzhitov, P Preston-Hurlburt, C A Janeway

ABSTRACT

Induction of the adaptive immune response depends on the expression of co-stimulatory molecules and cytokines by antigen-presenting cells. The mechanisms that control the initial induction of these signals upon infection are poorly understood. It has been proposed that their expression is controlled by the non-clonal, or innate, component of immunity that preceded in evolution the development of an adaptive immune system in vertebrates. We report here the cloning and characterization of a human homologue of the Drosophila toll protein (Toll) which has been shown to induce the innate immune response in adult Drosophila. Like Drosophila Toll, human Toll is a type I transmembrane protein with an extracellular domain consisting of a leucine-rich repeat (LRR) domain, and a cytoplasmic domain homologous to the cytoplasmic domain of the human interleukin (IL)-1 receptor. Both Drosophila Toll and the IL-1 receptor are known to signal through the NF-kappaB pathway. We show that a constitutively active mutant of human Toll transfected into human cell lines can induce the activation of NF-kappaB and the expression of NF-kappaB-controlled genes for the inflammatory cytokines IL-1, IL-6 and IL-8, as well as the expression of the co-stimulatory molecule B7.1, which is required for the activation of naive T cells. More... »

PAGES

394-397

References to SciGraph publications

  • 1991-05. Drosophila Toll and IL-1 receptor in NATURE
  • 1994-02. Issues in searching molecular sequence databases in NATURE GENETICS
  • 1994-01. Ancient relationships in NATURE
  • Journal

    TITLE

    Nature

    ISSUE

    6640

    VOLUME

    388

    Author Affiliations

    Clinical Trials linked to this publication

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  • Identifiers

    URI

    http://scigraph.springernature.com/pub.10.1038/41131

    DOI

    http://dx.doi.org/10.1038/41131

    DIMENSIONS

    https://app.dimensions.ai/details/publication/pub.1048300852

    PUBMED

    https://www.ncbi.nlm.nih.gov/pubmed/9237759


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    51 schema:description Induction of the adaptive immune response depends on the expression of co-stimulatory molecules and cytokines by antigen-presenting cells. The mechanisms that control the initial induction of these signals upon infection are poorly understood. It has been proposed that their expression is controlled by the non-clonal, or innate, component of immunity that preceded in evolution the development of an adaptive immune system in vertebrates. We report here the cloning and characterization of a human homologue of the Drosophila toll protein (Toll) which has been shown to induce the innate immune response in adult Drosophila. Like Drosophila Toll, human Toll is a type I transmembrane protein with an extracellular domain consisting of a leucine-rich repeat (LRR) domain, and a cytoplasmic domain homologous to the cytoplasmic domain of the human interleukin (IL)-1 receptor. Both Drosophila Toll and the IL-1 receptor are known to signal through the NF-kappaB pathway. We show that a constitutively active mutant of human Toll transfected into human cell lines can induce the activation of NF-kappaB and the expression of NF-kappaB-controlled genes for the inflammatory cytokines IL-1, IL-6 and IL-8, as well as the expression of the co-stimulatory molecule B7.1, which is required for the activation of naive T cells.
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