Back to all available

OX40-induced Th9 Cells leading to pancreatic acinar cell apoptosis via the STAT3/SOCS3 signaling pathway

emergency-and-critical-care
gastroenterology-and-hepatology
infectious-diseases

Abstract

Background. Severe acute Pancreatitis (SAP) is a severe subtype of Acute Pancreatitis (AP), characterized by extensive pancreatic necrosis, persistent organ failure, and systemic inflammatory response syndrome (SIRS), with a high mortality rate. Existing research indicates that Th9 cells play an important role in the early stage of AP and may be the key for AP to transform into SAP. However, the related mechanisms of Th9 cells in the early inflammatory response process of SAP still need further study.

Methods. We established an in vitro model of SAP in AR42J cells stimulated by Cerulein combined with Lipopolysaccharide (LPS) and co-cultured it with Ox40-induced Th9 cells that only produced interleukin 9 (IL-9) to clarify the role of Th9/IL-9 cells and their related suppressor of cytokine signaling 3(SOCS3)/signal transducer and activator of transcription 3 (STAT3) signaling pathway in the early stage of SAP.

Results. In this study, IL-9, secreted in large quantities by Th9 cells, reduced the generation of SCOS3, exacerbated the phosphorylation of STAT3, and led to an increase in the secretion of the pro-inflammatory factor interleukin 6 (IL-6) and tumor necrosis factor-α (TNF-α), as well as an increase in the apoptosis of AR42J cells. Over-expressing SCOS3 could significantly reverse this change.

Conclusion. This study shows that OX40-induced Th9 cells lead to a large secretion of IL-9, cause inflammatory factor storm, and aggravate the apoptosis of AR42J cells via the STAT3/SOCS3 signaling pathway.

Ask to review this manuscript

Notes for potential reviewers

  • Volunteering is not a guarantee that you will be asked to review. There are many reasons: reviewers must be qualified, there should be no conflicts of interest, a minimum of two reviewers have already accepted an invitation, etc.
  • This is NOT OPEN peer review. The review is single-blind, and all recommendations are sent privately to the Academic Editor handling the manuscript. All reviews are published and reviewers can choose to sign their reviews.
  • What happens after volunteering? It may be a few days before you receive an invitation to review with further instructions. You will need to accept the invitation to then become an official referee for the manuscript. If you do not receive an invitation it is for one of many possible reasons as noted above.
  • PeerJ does not judge submissions based on subjective measures such as novelty, impact or degree of advance. Effectively, reviewers are asked to comment on whether or not the submission is scientifically and technically sound and therefore deserves to join the scientific literature. Our Peer Review criteria can be found on the "Editorial Criteria" page - reviewers are specifically asked to comment on 3 broad areas: "Basic Reporting", "Experimental Design" and "Validity of the Findings".
  • Reviewers are expected to comment in a timely, professional, and constructive manner.
  • Until the article is published, reviewers must regard all information relating to the submission as strictly confidential.
  • When submitting a review, reviewers are given the option to "sign" their review (i.e. to associate their name with their comments). Otherwise, all review comments remain anonymous.
  • All reviews of published articles are published. This includes manuscript files, peer review comments, author rebuttals and revised materials.
  • Each time a decision is made by the Academic Editor, each reviewer will receive a copy of the Decision Letter (which will include the comments of all reviewers).

If you have any questions about submitting your review, please email us at [email protected].