AI Article Synopsis
- * In a study, researchers found that genes activated by type I interferon (T1IFN) are more active in ILC2s during colitis induced by DSS, and this signaling leads to lower production of certain cytokines.
- * Blocking T1IFN signaling worsens colitis symptoms in mice, indicating that T1IFN plays a protective role in ILC2s during inflammation, with a link to a protein called amphiregulin (AREG), which may help mitigate colitis when supplemented.
Article Abstract
Group 2 innate lymphoid cells (ILC2s) serve as frontline defenses against parasites. However, excluding helminth infections, it is poorly understood how ILC2s function in intestinal inflammation, including inflammatory bowel disease.Here, we analyzed the global gene expression of ILC2s in healthy and colitic conditions and revealed that type I interferon (T1IFN)-stimulated genes were up-regulated in ILC2s in dextran sodium sulfate (DSS)-induced colitis. The enhancement of T1IFN signaling in ILC2s in DSS-induced colitis was correlated with the downregulation of cytokine production by ILC2s, such as interleukin-5. Blocking T1IFN signaling during colitis resulted in exaggeration of colitis in both wild-type and -deficient mice. The exacerbation of colitis induced by neutralization of T1IFN signaling was accompanied by reduction of amphiregulin (AREG) in ILC2s and was partially rescued by exogenous AREG treatment. Collectively, these findings show the potential roles of T1IFN in ILC2s that contribute to colitis manifestation.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9578145 | PMC |
| http://dx.doi.org/10.3389/fimmu.2022.982827 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Olaparib and Radiotherapy Induce Type I Interferon- and CD8+ T Cell-Dependent Sensitization to Immunotherapy in Pancreatic Cancer.
Mol Cancer Ther
December 2024
Department of Radiation Oncology, University of Michigan Rogel Cancer Center, Ann Arbor, Michigan.
PARP inhibitors sensitize pancreatic ductal adenocarcinoma (PDAC) to radiation by inducing DNA damage and replication stress. These mechanisms also have the potential to enhance radiation-induced type I interferon (T1IFN)-mediated antitumoral immune responses. We hypothesized that the PARP inhibitor olaparib would also potentiate radiation-induced T1IFN to promote antitumor immune responses and sensitization of otherwise resistant PDAC to immunotherapy.
View Article and Find Full Text PDFLoss of the DNA repair protein, polynucleotide kinase/phosphatase, activates the type 1 interferon response independent of ionizing radiation.
Nucleic Acids Res
September 2024
Department of Oncology, University of Alberta, Edmonton, Alberta T6G 2R3, Canada.
DNA damage has been implicated in the stimulation of the type 1 interferon (T1IFN) response. Here, we show that downregulation of the DNA repair protein, polynucleotide kinase/phosphatase (PNKP), in a variety of cell lines causes robust phosphorylation of STAT1, upregulation of interferon-stimulated genes and persistent accumulation of cytosolic DNA, all of which are indicators for the activation of the T1IFN response. Furthermore, this did not require damage induction by ionizing radiation.
View Article and Find Full Text PDFPotentiating the radiation-induced type I interferon antitumoral immune response by ATM inhibition in pancreatic cancer.
JCI Insight
February 2024
Department of Radiation Oncology and.
Article Synopsis
- Radiotherapy can trigger a type I interferon-mediated immune response, which may be strengthened by a new ATM inhibitor, enhancing the body's antitumoral efforts against pancreatic cancer.
- Experiments with the ATM inhibitors AZD1390 and AZD0156 revealed that they boost radiation-induced type I interferon expression through specific immune signaling pathways.
- In mouse models, the combination of ATM inhibitors and radiotherapy improved immune responses, leading to better tumor control, increased CD8+ T cell activity, and the potential for effective systemic treatments against other tumors outside the radiation zone.
Epithelially Restricted Interferon Epsilon Protects Against Colitis.
Cell Mol Gastroenterol Hepatol
January 2024
Centre for Innate Immunity and Infectious Diseases, Hudson Institute of Medical Research, Clayton, VIC, Australia; Department of Molecular and Translational Sciences, Monash University, Clayton, VIC, Australia.
Background & Aims: Type I interferon (T1IFN) signalling is crucial for maintaining intestinal homeostasis. We previously found that the novel T1IFN, IFNε, is highly expressed by epithelial cells of the female reproductive tract, where it protects against pathogens. Its function has not been studied in the intestine.
View Article and Find Full Text PDFEnrichment of type I interferon signaling in colonic group 2 innate lymphoid cells in experimental colitis.
Front Immunol
October 2022
Division of Gastroenterology and Hepatology, Department of Internal Medicine, School of Medicine, Keio University, Tokyo, Japan.
Article Synopsis
- * In a study, researchers found that genes activated by type I interferon (T1IFN) are more active in ILC2s during colitis induced by DSS, and this signaling leads to lower production of certain cytokines.
- * Blocking T1IFN signaling worsens colitis symptoms in mice, indicating that T1IFN plays a protective role in ILC2s during inflammation, with a link to a protein called amphiregulin (AREG), which may help mitigate colitis when supplemented.
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!