ArticleProceedings of the National Academy of Sciences of the United States of America2022
Injury-induced inflammatory signaling and hematopoiesis in
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 45 citations in OpenAlex.
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- Dual role of PpV in Drosophila crystal cell proliferation and survival.Journal of molecular cell biology · 2025Article
- Encapsulation and Melanization Are Not Correlated to Successful Immune Defense Against Parasitoid Wasps inCells · 2025Article
- A novel role for Hsc70-4 in blood cell differentiation inFrontiers in immunology · 2025Article
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- MdSVWC1, a new pattern recognition receptor triggers multiple defense mechanisms against invading bacteria in Musca domestica.BMC biology · 2024Article
- Wnt signaling couples G2 phase control with differentiation during hematopoiesis in Drosophila.Developmental cell · 2024Article
- Formation of recurring transient CaProceedings of the National Academy of Sciences of the United States of America · 2024Article
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- Editorial: Community series in recent advances inFrontiers in immunology · 2024Article
- LPS adsorption and inflammation alleviation by polymyxin B-modified liposomes for atherosclerosis treatment.Acta pharmaceutica Sinica. B · 2023Article
- Damage sensing mediated by serine proteases Hayan and Persephone for Toll pathway activation in apoptosis-deficient flies.PLoS genetics · 2023Article
- A mechanosensitive vascular niche forProceedings of the National Academy of Sciences of the United States of America · 2023Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Inflammatory response in Drosophila to sterile (axenic) injury in embryos and adults has received some attention in recent years, and most concentrate on the events at the injury site. Here we focus on the effect sterile injury has on the hematopoietic organ, the lymph gland, and the circulating blood cells in the larva, the developmental stage at which major events of hematopoiesis are evident. In mammals, injury activates Toll-like receptor/NF-κB signaling in macrophages, which then express and secrete secondary, proinflammatory cytokines. In Drosophila larvae, distal puncture injury of the body wall epidermis causes a rapid activation of Toll and Jun kinase (JNK) signaling throughout the hematopoietic system and the differentiation of a unique blood cell type, the lamellocyte. Furthermore, we find that Toll and JNK signaling are coupled in their activation. Secondary to this Toll/JNK response, a cytokine, Upd3, is induced as a Toll pathway transcriptional target, which then promotes JAK/STAT signaling within the blood cells. Toll and JAK/STAT signaling are required for the emergence of the injury-induced lamellocytes. This is akin to the derivation of specialized macrophages in mammalian systems. Upstream, at the injury site, a Duox- and peroxide-dependent signal causes the activation of the proteases Grass and SPE, needed for the activation of the Toll-ligand Spz, but microbial sensors or the proteases most closely associated with them during septic injury are not involved in the axenic inflammatory response.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.