Earthworm leukocytes kill HeLa, HEp-2, PC-12 and PA317 cells in vitro

Engelmann, Péter; Kiss, Judit; Csöngei, Veronika; Cooper, Edwin L.; Németh, Pèter

doi:10.1016/j.jbbm.2004.04.004

Cited by 35 publications

(30 citation statements)

References 32 publications

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“…There is evidence for cells with NK properties in the tunicate Botryllus schlosseri , and the Ciona intestinalis genome includes homologs of some NK cell receptors [5,8]. More basic cytotoxic NK-like cells have been described in earlier divergent invertebrates such as earthworms [9]. How similar these cells are to conventional mammalian NKs, including their mechanisms of killing, remains to be seen.…”

Section: Introductionmentioning

confidence: 99%

Perforin evolved from a gene duplication of MPEG1, followed by a complex pattern of gene gain and loss within Euteleostomi

et al. 2012

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BackgroundThe pore-forming protein perforin is central to the granule-exocytosis pathway used by cytotoxic lymphocytes to kill abnormal cells. Although this mechanism of killing is conserved in bony vertebrates, cytotoxic cells are present in other chordates and invertebrates, and their cytotoxic mechanism has not been elucidated. In order to understand the evolution of this pathway, here we characterize the origins and evolution of perforin.ResultsWe identified orthologs and homologs of human perforin in all but one species analysed from Euteleostomi, and present evidence for an earlier ortholog in Gnathostomata but not in more primitive chordates. In placental mammals perforin is a single copy gene, but there are multiple perforin genes in all lineages predating marsupials, except birds. Our comparisons of these many-to-one homologs of human perforin show that they mainly arose from lineage-specific gene duplications in multiple taxa, suggesting acquisition of new roles or different modes of regulation. We also present evidence that perforin arose from duplication of the ancient MPEG1 gene, and that it shares a common ancestor with the functionally related complement proteins.ConclusionsThe evolution of perforin in vertebrates involved a complex pattern of gene, as well as intron, gain and loss. The primordial perforin gene arose at least 500 million years ago, at around the time that the major histocompatibility complex-T cell receptor antigen recognition system was established. As it is absent from primitive chordates and invertebrates, cytotoxic cells from these lineages must possess a different effector molecule or cytotoxic mechanism.

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Section: Introductionmentioning

confidence: 99%

Perforin evolved from a gene duplication of MPEG1, followed by a complex pattern of gene gain and loss within Euteleostomi

et al. 2012

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“…Certain molecules from the coelomic fluid inhibit bacterial growth and lyse various mammalian red blood cells (Engelmann et al, 2004a).…”

Section: Introductionmentioning

confidence: 99%

Activity and immunodetection of lysozyme in earthworm Dendrobaena veneta (Annelida)

Fiołka

Zagaja

Hułas-Stasiak

et al. 2012

Journal of Invertebrate Pathology

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“…Lending more credence to blurring, Kvell et al have reached similar conclusions from a group, unlike others, consisting of a mix of vertebrate and invertebrate immunologists with particular emphasis on earthworms [2,[87][88][89][90][91][92]. Adaptive immunity has often been considered the penultimate of immune capacities.…”

Section: A Viewpoint From Earthworm Immunologistsmentioning

confidence: 89%

Evolution of immune systems from self/not self to danger to artificial immune systems (AIS)

Cooper

2010

Physics of Life Reviews

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Earthworm leukocytes kill HeLa, HEp-2, PC-12 and PA317 cells in vitro

Cited by 35 publications

References 32 publications

Perforin evolved from a gene duplication of MPEG1, followed by a complex pattern of gene gain and loss within Euteleostomi

Perforin evolved from a gene duplication of MPEG1, followed by a complex pattern of gene gain and loss within Euteleostomi

Activity and immunodetection of lysozyme in earthworm Dendrobaena veneta (Annelida)

Evolution of immune systems from self/not self to danger to artificial immune systems (AIS)

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