Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Bacillus anthracis lethal toxin negatively modulates ILC3 function through perturbation of IL-23-mediated MAPK signaling

23 Oct 2017

Abstract excerpt

Bacillus anthracis, the causative agent of anthrax, secretes lethal toxin that down-regulates immune functions.Translocation of B. anthracis across mucosal epithelia is key for its dissemination and pathogenesis.Group 3 innate lymphocytes (ILC3s) are important in mucosal barrier maintenance due to their expression of the cytokine IL-22, a critical regulator of tissue responses and repair during homeostasis and...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to IL-33, ST2, and ILC Pathways
Share to Transgenic Plants and Applications
Share to Viral gastroenteritis research and epidemiology

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 29059238
DOI: 10.1371/journal.ppat.1006690

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Bacillus anthracis lethal toxin negatively modulates ILC3 function through perturbation of IL-23-mediated MAPK signalingPMID 29059238Read ↗

An anthrax lethal factor mutant that is defective at causing pyroptosis retains proapoptotic activity.Semantic proximity Read ↗

Anthrax Lethal Toxin-Mediated Killing of Human and Murine Dendritic Cells Impairs the Adaptive Immune ResponseSemantic proximity Read ↗

Anthrax lethal toxin-induced inflammasome formation and caspase-1 activation are late events dependent on ion fluxes and the proteasome.Semantic proximity Read ↗

Anthrax toxin induces macrophage death by p38 MAPK inhibition but leads to inflammasome activation via ATP leakage.Semantic proximity Read ↗

Cutting edge: resistance to Bacillus anthracis infection mediated by a lethal toxin sensitive allele of Nalp1b/Nlrp1b.Semantic proximity Read ↗

Anthrax lethal toxin paralyzes actin-based motility by blocking Hsp27 phosphorylation.Semantic proximity Read ↗

Staphylococcal enterotoxin A (SEA) stimulates STAT3 activation and IL-17 expression in cutaneous T-cell lymphomaSemantic proximity Read ↗

Escherichia coli heat-labile enterotoxin promotes protective Th17 responses against infection by driving innate IL-1 and IL-23 production.Semantic proximity Read ↗

Identification of Novel Host-Targeted Compounds That Protect from Anthrax Lethal Toxin-Induced Cell DeathSemantic proximity Read ↗

Inhibition of Interleukin 1β (IL-1β) Expression by Anthrax Lethal Toxin (LeTx) Is Reversed by Histone Deacetylase 8 (HDAC8) Inhibition in Murine MacrophagesSemantic proximity Read ↗

EST-based genome-wide gene inactivation identifies ARAP3 as a host protein affecting cellular susceptibility to anthrax toxinSemantic proximity Read ↗

Calcium-dependent plasma membrane binding and cell lysis by perforin are mediated through its C2 domain: A critical role for aspartate residues 429, 435, 483, and 485 but not 491.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.