| First Author | Yamamoto K | Year | 2021 |
| Journal | iScience | Volume | 24 |
| Issue | 9 | Pages | 103064 |
| PubMed ID | 34585114 | Mgi Jnum | J:313362 |
| Mgi Id | MGI:6798053 | Doi | 10.1016/j.isci.2021.103064 |
| Citation | Yamamoto K, et al. (2021) The TLR4-TRIF-type 1 IFN-IFN-gamma pathway is crucial for gastric MALT lymphoma formation after Helicobacter suis infection. iScience 24(9):103064 |
| abstractText | Helicobacter suis, a zoonotic infection-related bacterium, can induce gastric mucosa-associated lymphoid tissue (MALT) lymphoma in humans and animals. Recently, we reported that the formation of gastric MALT lymphoma after H. suis infection is induced by interferon (IFN)-gamma activation. Here, we revealed that activation of the Toll-like receptor (TLR) 4-Toll/IL-1 receptor domain-containing adapter-inducing interferon-beta (TRIF) pathway after H. suis infection is associated with the production of type 1 IFNs (IFN-alpha, IFN-beta) by gastric epithelial cells. Additionally, these type 1 IFNs interact with type 1 IFN receptors on gastric B cells, facilitating the secretion of IFN-gamma and the activation of which is enhanced by positive feedback regulation in B cells. These results suggest that the TLR4-TRIF-type 1 IFN-IFN-gamma pathway is crucial in the development of gastric MALT lymphoma after H. suis infection and may, therefore, represent a therapeutic target for the prevention of this condition. |
