ORCID Profile
0000-0001-8326-6645
Current Organisations
Universidade Católica Portuguesa, Faculdade de Medicina, Católica Biomedical Research Centre
,
Instituto Gulbenkian de Ciência
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Publisher: Public Library of Science (PLoS)
Date: 09-06-2014
Publisher: eLife Sciences Publications, Ltd
Date: 24-10-2016
Publisher: eLife Sciences Publications, Ltd
Date: 21-09-2018
Publisher: eLife Sciences Publications, Ltd
Date: 27-09-2018
DOI: 10.7554/ELIFE.38636
Abstract: Damage-associated molecular patterns (DAMPs) are molecules exposed or released by dead cells that trigger or modulate immunity and tissue repair. In vertebrates, the cytoskeletal component F-actin is a DAMP specifically recognised by DNGR-1, an innate immune receptor. Previously we suggested that actin is also a DAMP in Drosophila melanogaster by inducing STAT-dependent genes ( xref ref-type="bibr" rid="bib10" Srinivasan et al., 2016 /xref ). Here, we revise that conclusion and report that α-actinin is far more potent than actin at inducing the same STAT response and can be found in trace amounts in actin preparations. Recombinant expression of actin or α-actinin in bacteria demonstrated that only α-actinin could drive the expression of STAT target genes in Drosophila. The response to injected α-actinin required the same signalling cascade that we had identified in our previous work using actin preparations. Taken together, these data indicate that α-actinin rather than actin drives STAT activation when injected into Drosophila.
Publisher: eLife Sciences Publications, Ltd
Date: 22-11-2016
DOI: 10.7554/ELIFE.19662
Abstract: Damage-associated molecular patterns (DAMPs) are molecules released by dead cells that trigger sterile inflammation and, in vertebrates, adaptive immunity. Actin is a DAMP detected in mammals by the receptor, DNGR-1, expressed by dendritic cells (DCs). DNGR-1 is phosphorylated by Src-family kinases and recruits the tyrosine kinase Syk to promote DC cross-presentation of dead cell-associated antigens. Here we report that actin is also a DAMP in invertebrates that lack DCs and adaptive immunity. Administration of actin to Drosophila melanogaster triggers a response characterised by selective induction of STAT target genes in the fat body through the cytokine Upd3 and its JAK/STAT-coupled receptor, Domeless. Notably, this response requires signalling via Shark, the Drosophila orthologue of Syk, and Src42A, a Drosophila Src-family kinase, and is dependent on Nox activity. Thus, extracellular actin detection via a Src-family kinase-dependent cascade is an ancient means of detecting cell injury that precedes the evolution of adaptive immunity.
Location: United Kingdom of Great Britain and Northern Ireland
Location: Portugal
Location: Portugal
No related grants have been discovered for Luis Teixeira.