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

Cutting Edge: IL-1 Controls the IL-23 Response Induced by Gliadin, the Etiologic Agent in Celiac Disease

1 Oct 2008

Abstract excerpt

IL-23 has been implicated in the pathogenesis of several tissue-specific autoimmune diseases. Currently, celiac disease (CD) is the only autoimmune disease in which both the major genetic (95% HLA-DQ2(+)) and etiologic factors (dietary glutens) for susceptibility are known. We demonstrate that wheat gliadin induces significantly greater production of IL-23, IL-1beta, and TNF-alpha in PBMC from CD patients...

Read the complete abstract on PubMed

Topics

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

Share to Celiac Disease Research and Management
Share to Microscopic Colitis
Share to Whipple's Disease and Interleukins

Methodology Data sources Editorial policy Privacy Delete account & data About Contact Helena Bioinformatics

Source

Identifiers

PMID: 18802048
DOI: 10.4049/jimmunol.181.7.4457

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 8 closest

Cutting Edge: IL-1 Controls the IL-23 Response Induced by Gliadin, the Etiologic Agent in Celiac DiseasePMID 18802048Read ↗

Systems-level analysis of monocyte responses in inflammatory bowel disease identifies IL-10 and IL-1 cytokine networks that regulate IL-23Semantic proximity Read ↗

Glucose-Responsive CD20+ Cytotoxic T Cells: A Novel Pro-inflammatory Mediator in the Immunopathogenesis of Type 2 DiabetesSemantic proximity Read ↗

T <sub>H</sub> 17 (and T <sub>H</sub> 1) signatures of intestinal biopsies of CD patients in response to gliadinSemantic proximity Read ↗

Cutting Edge: IFN-γ Is a Negative Regulator of IL-23 in Murine Macrophages and Experimental ColitisSemantic proximity Read ↗

Gliadin as a stimulator of innate responses in celiac diseaseSemantic proximity Read ↗

Induction of a colitogenic phenotype in Th1 cells depends on IL-23R signalingSemantic proximity Read ↗

In vitro differentiation of human monocytes into dendritic cells by peptic-tryptic digest of gliadin is independent of genetic predisposition and the presence of celiac disease.Semantic proximity Read ↗

Pouring fuel on the fire: Th17 cells, the environment, and autoimmunitySemantic proximity Read ↗

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