ArticlePLoS biology2018
Dectin-1/2-induced autocrine PGE2 signaling licenses dendritic cells to prime Th2 responses.
Article in PLoS biology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 79 citations in OpenAlex.
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- Advances in new target molecules against schistosomiasis: A comprehensive discussion of physiological structure and nutrient intake.PLoS pathogens · 2023Review
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- Immunological mechanisms involved in macrophage activation and polarization in schistosomiasis.Parasitology · 2023Review
- Blocking Dectin-1 prevents colorectal tumorigenesis by suppressing prostaglandin E2 production in myeloid-derived suppressor cells and enhancing IL-22 binding protein expression.Nature communications · 2023Article
- The Immune Response to Nematode Infection.International journal of molecular sciences · 2023Review
- How to train your myeloid cells: a way forward for helminth vaccines?Frontiers in immunology · 2023Review
- The immunoregulatory effect of the TREM2-agonist Sulfavant A in human allogeneic mixed lymphocyte reaction.Frontiers in immunology · 2023Article
- The kinase p38α functions in dendritic cells to regulate Th2-cell differentiation and allergic inflammation.Cellular & molecular immunology · 2022Article
- Helminthic dehydrogenase drives PGEEMBO reports · 2022Article
- Inhibition of COX-2 ameliorates murine liver schistosomiasis japonica through splenic cellular immunoregulation.Parasites & vectors · 2022Article
- β-Glucan receptors on IL-4 activated macrophages are required for hookworm larvae recognition and trapping.Immunology and cell biology · 2022Article
Corrections and comments
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Authors and funding
13 authors at 6 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The molecular mechanisms through which dendritic cells (DCs) prime T helper 2 (Th2) responses, including those elicited by parasitic helminths, remain incompletely understood. Here, we report that soluble egg antigen (SEA) from Schistosoma mansoni, which is well known to drive potent Th2 responses, triggers DCs to produce prostaglandin E2 (PGE2), which subsequently-in an autocrine manner-induces OX40 ligand (OX40L) expression to license these DCs to drive Th2 responses. Mechanistically, SEA was found to promote PGE2 synthesis through Dectin-1 and Dectin-2, and via a downstream signaling cascade involving spleen tyrosine kinase (Syk), extracellular signal-regulated kinase (ERK), cytosolic phospholipase A2 (cPLA2), and cyclooxygenase 1 and 2 (COX-1 and COX-2). In addition, this pathway was activated independently of the actions of omega-1 (ω-1), a previously described Th2-priming glycoprotein present in SEA. These findings were supported by in vivo murine data showing that ω-1-independent Th2 priming by SEA was mediated by Dectin-2 and Syk signaling in DCs. Finally, we found that Dectin-2-/-, and to a lesser extent Dectin-1-/- mice, displayed impaired Th2 responses and reduced egg-driven granuloma formation following S. mansoni infection, highlighting the physiological importance of this pathway in Th2 polarization during a helminth infection. In summary, we identified a novel pathway in DCs involving Dectin-1/2-Syk-PGE2-OX40L through which Th2 immune responses are induced.
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