ArticleEMBO reports2021
The UPR sensor IRE1α promotes dendritic cell responses to control Toxoplasma gondii infection.
Article in EMBO reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Intracellular pathogen manipulation of ER-phagy: direct receptor targeting and indirect pathway perturbation.Medical microbiology and immunology · 2026Review
- Metabolic reprogramming of immune cells in the battle against intracellular bacterial chronic infections: novel mechanisms and breakthroughs.Molecular biology reports · 2025Review
- Lipid nanoparticles as a tool to dissect dendritic cell maturation pathways.Cell reports · 2025Article
- Endoplasmic reticulum stress-a key guardian in cancer.Cell death discovery · 2024Review
- Emerging mechanisms of the unfolded protein response in therapeutic resistance: from chemotherapy to Immunotherapy.Cell communication and signaling : CCS · 2024Review
- Toxoplasma-host endoplasmic reticulum interaction: HowCurrent research in microbial sciences · 2024Review
- The Unfolded Protein Response Sensor IRE1 Regulates Activation of In Vitro Differentiated Type 1 Conventional DCs with Viral Stimuli.International journal of molecular sciences · 2023Article
- Traditional Chinese medicines and natural products targeting immune cells in the treatment of metabolic-related fatty liver disease.Frontiers in pharmacology · 2023Review
- Antigen-derived peptides engage the ER stress sensor IRE1α to curb dendritic cell cross-presentation.The Journal of cell biology · 2022Article
- The UPR sensor IRE1α promotes dendritic cell responses to control Toxoplasma gondii infection.EMBO reports · 2021Article
- Endoplasmic Reticulum Stress, a Target for Drug Design and Drug Resistance in Parasitosis.Frontiers in microbiology · 2021Review
Corrections and comments
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
The unfolded protein response (UPR) has emerged as a central regulator of immune cell responses in several pathologic contexts including infections. However, how intracellular residing pathogens modulate the UPR in dendritic cells (DCs) and thereby affect T cell-mediated immunity remains uncharacterized. Here, we demonstrate that infection of DCs with Toxoplasma gondii (T. gondii) triggers a unique UPR signature hallmarked by the MyD88-dependent activation of the IRE1α pathway and the inhibition of the ATF6 pathway. Induction of XBP1s controls pro-inflammatory cytokine secretion in infected DCs, while IRE1α promotes MHCI antigen presentation of secreted parasite antigens. In mice, infection leads to a specific activation of the IRE1α pathway, which is restricted to the cDC1 subset. Mice deficient for IRE1α and XBP1 in DCs display a severe susceptibility to T. gondii and succumb during the acute phase of the infection. This early mortality is correlated with increased parasite burden and a defect in splenic T-cell responses. Thus, we identify the IRE1α/XBP1s branch of the UPR as a key regulator of host defense upon T. gondii infection.
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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.