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Drosophila cellular immunity: a story of migration and adhesion
CEA, Institut de Recherches en Technologies et Sciences pour le Vivant, Laboratoire de Biologie à Grande Echelle, F-38054 Grenoble, France.
Institute of Biological and Environmental Sciences, University of Aberdeen, Aberdeen AB24 2TZ, UK .
2011 (English)In: Journal of Cell Science, ISSN 0021-9533, E-ISSN 1477-9137, Vol. 124, no 9, 1373-1382 p.Article in journal (Refereed) Published
Abstract [en]

Research during the past 15 years has led to significant breakthroughs, providing evidence of a high degree of similarity between insect and mammalian innate immune responses, both humoural and cellular, and highlighting Drosophila melanogaster as a model system for studying the evolution of innate immunity. In a manner similar to cells of the mammalian monocyte and macrophage lineage, Drosophila immunosurveillance cells (haemocytes) have a number of roles. For example, they respond to wound signals, are involved in wound healing and contribute to the coagulation response. Moreover, they participate in the phagocytosis and encapsulation of invading pathogens, are involved in the removal of apoptotic bodies and produce components of the extracellular matrix. There are several reasons for using the Drosophila cellular immune response as a model to understand cell signalling during adhesion and migration in vivo: many genes involved in the regulation of Drosophila haematopoiesis and cellular immunity have been maintained across taxonomic groups ranging from flies to humans, many aspects of Drosophila and mammalian innate immunity seem to be conserved, and Drosophila is a simplified and well-studied genetic model system. In the present Commentary, we will discuss what is known about cellular adhesion and migration in the Drosophila cellular immune response, during both embryonic and larval development, and where possible compare it with related mechanisms in vertebrates.

Place, publisher, year, edition, pages
2011. Vol. 124, no 9, 1373-1382 p.
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URN: urn:nbn:se:uu:diva-161627DOI: 10.1242/jcs.064592PubMedID: 21502134OAI: oai:DiVA.org:uu-161627DiVA: diva2:497077
Available from: 2012-02-10 Created: 2011-11-15 Last updated: 2013-03-13Bibliographically approved

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Williams, Michael J
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