Control of Drosophila blood cell activation via Toll signaling in the fat body

PLoS One. 2014 Aug 7;9(8):e102568. doi: 10.1371/journal.pone.0102568. eCollection 2014.

Abstract

The Toll signaling pathway, first discovered in Drosophila, has a well-established role in immune responses in insects as well as in mammals. In Drosophila, the Toll-dependent induction of antimicrobial peptide production has been intensely studied as a model for innate immune responses in general. Besides this humoral immune response, Toll signaling is also known to activate blood cells in a reaction that is similar to the cellular immune response to parasite infections, but the mechanisms of this response are poorly understood. Here we have studied this response in detail, and found that Toll signaling in several different tissues can activate a cellular immune defense, and that this response does not require Toll signaling in the blood cells themselves. Like in the humoral immune response, we show that Toll signaling in the fat body (analogous to the liver in vertebrates) is of major importance in the Toll-dependent activation of blood cells. However, this Toll-dependent mechanism of blood cell activation contributes very little to the immune response against the parasitoid wasp, Leptopilina boulardi, probably because the wasp is able to suppress Toll induction. Other redundant pathways may be more important in the defense against this pathogen.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Drosophila / immunology*
  • Drosophila / metabolism
  • Drosophila / parasitology
  • Drosophila Proteins / genetics
  • Drosophila Proteins / metabolism
  • Drosophila Proteins / physiology*
  • Fat Body / metabolism*
  • Hemocytes / metabolism*
  • Host-Parasite Interactions / immunology*
  • Immunity, Cellular*
  • Larva / immunology*
  • Larva / metabolism
  • Larva / parasitology
  • Signal Transduction
  • Toll-Like Receptors / genetics
  • Toll-Like Receptors / metabolism
  • Toll-Like Receptors / physiology*
  • Wasps / physiology

Substances

  • Drosophila Proteins
  • Tl protein, Drosophila
  • Toll-Like Receptors

Grant support

This work was supported by the Swedish Research Council, the Swedish Cancer Society and the Sigrid Juselius Foundation to DH, the Academy of Finland to DH and MR, and Competitive Research Funding of the Tampere University Hospital to MR. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.