ArticleFrontiers in microbiology2015
Pasteurella multocida Toxin Manipulates T Cell Differentiation.
Article in Frontiers in microbiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed, 20 citations in OpenAlex.
- Th17 cells/IL-17A shape Pasteurella multocida serotype A infection in murine and rabbit models.Veterinary research · 2025Article
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- Development of a detection chip for major pathogenic drug-resistant genes and drug targets in bovine respiratory system diseases.Open life sciences · 2024Article
- A multi-omic analysis reveals the esophageal dysbiosis as the predominant trait of eosinophilic esophagitis.Journal of translational medicine · 2023Article
- Bloodstream infection, peritonitis, and pneumonia caused byFrontiers in cellular and infection microbiology · 2023Review
- Pasteurella multocida toxin - lessons learned from a mitogenic toxin.Frontiers in immunology · 2022Review
- PIM Kinases in Multiple Myeloma.Cancers · 2021Review
- The cancer metabolic reprogramming and immune response.Molecular cancer · 2021Review
- Oral and intestinal bacterial exotoxins: Potential linked to carcinogenesis.Progress in molecular biology and translational science · 2020Review
- Transcriptomic Analysis of Chicken Lungs Infected With Avian and BovineFrontiers in veterinary science · 2020Article
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- Transcriptomic Analysis on Responses of Murine Lungs toFrontiers in cellular and infection microbiology · 2017Article
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Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Pasteurella multocida causes various diseases in a broad range of wild and domestic animals. Toxigenic strains of the serotypes A and D produce an AB protein toxin named Pasteurella multocida toxin (PMT). PMT constitutively activates the heterotrimeric G protein subunits Gαq, Gα13, and Gαi through deamidation of a glutamine residue, which results in cytoskeletal rearrangements as well as increased proliferation and survival of the host cell. In human monocytes, PMT alters the lipopolysaccharide (LPS)-induced activation toward a phenotype that suppresses T cell activation. Here we describe that the toxin also modulates CD4-positive T helper (Th) cells directly. PMT amplifies the expansion of Th cells through enhanced cell cycle progression and suppression of apoptosis and manipulates the differentiation of Th subclasses through activation of Signal Transducers and Activators of Transcription (STAT) family members and induction of subtype-specific master transcription factors. A large population of toxin-treated T cells is double-positive for Foxp3 and RORγt, the transcription factors expressed by Treg and Th17 cells, respectively. This suggests that these cells could have the potential to turn into Th17 cells or suppressive Treg cells. However, in terms of function, the PMT-differentiated cells behave as inflammatory Th17 cells that produce IL-17 and trigger T cell proliferation.
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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.