Major upper gastrointestinal surgery is associated with an antigen-dependent proinflammatory T cell response
✍ Scribed by K. J. Sweeney; M. R. Kell; N. Ravi; J. V. Reynolds
- Publisher
- John Wiley and Sons
- Year
- 2005
- Tongue
- English
- Weight
- 127 KB
- Volume
- 92
- Category
- Article
- ISSN
- 0007-1323
- DOI
- 10.1002/bjs.4844
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Background
T cells play a central role in the immune response to injury. Oesophageal and pancreatic resections are associated with significant risk of systemic inflammatory response syndrome and sepsis. This study involved a detailed analysis of T cell function in a consecutive cohort of patients undergoing such surgery.
Methods
Twenty-five patients undergoing major oncological upper gastrointestinal surgery were investigated for T cell expression of Fas and the activation markers CD69 and CD25, as well as interleukin (IL) 2, IL-10 and interferon (IFN) γ responses to stimulation with staphylococcal enterotoxin B (SEB). T cell activation in healthy volunteer peripheral blood mononuclear cells was studied in co-culture with patients' serum, either alone or with cytotoxic T lymphocyte-associated antigen (CTLA) 4, an inhibitor of antigen presentation.
Results
T cells expressed significantly raised levels of CD69 and CD25 after surgery, but no change in Fas expression was evident. There was a significant increase in the production of IL-2 after surgery without a concomitant increase in IFN-γ or IL-10 in response to SEB. Postoperative serum activated healthy volunteer T cells, a response that was inhibited (P = 0·053) by co-incubation with CTLA-4.
Conclusion
Major surgery results in pan-T cell activation via a serum-mediated antigenic mechanism that is independent of Fas expression. Postoperative T cells are primed for an augmented proinflammatory response to superantigen, sustained for at least 1 week, implicating the adaptive immune system in the development of the postoperative systemic immunoinflammatory state.