Role of t cells for cytokine production and outcome in a model of acute septic peritonitis

Daniel Reim, Kay Westenfelder, Simone Kaiser-Moore, Sylvia Schlautkötter, Bernhard Holzmann, Heike Weiahardt

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


Although it is generally accepted that early defense mechanisms are controlled by cells of the innate immune system, T cells were found to be crucial for host resistance against acute septic peritonitis. However, the mechanisms by which T cells mediate protection are not fully understood. Here, we demonstrate mice deficient for recombinase-activating gene (RAG) 1, which lack mature B and T cells, showed enhanced susceptibility and impaired bacterial clearance in a model of acute septic peritonitis. Whereas B-cell-deficient p.MT mice showed no significant difference in the survival rate after peritonitis induction, T-cell-deficient Balb/c nude mice exhibited reduced survival. Importantly, analysis of cytokine production in both fMG-J-deficient and T-cell-deficient nude mice indicated strongly attenuated production of IL-12, interferon (IFN) γ, and IL-10 during sepsis. Reduced cytokine levels were detected both in serum and in organ extracts of septic mice. Direct analysis of T cells isolated from septic mice demonstrated that T cells respond to an acute septic challenge by increased production of IFN-γ and IL-10. Moreover, bacterial numbers in spleens of septic RAG-/-deficient mice were significantly increased as compared with controls, suggesting that T cells are engaged in the early antibacterial immune defense during sepsis, possibly via the production of IFN-γ. In summary, these results imply that T cells contribute to protective immune responses against acute systemic infections via their ability to produce crucial immune mediators.

Original languageEnglish
Pages (from-to)245-250
Number of pages6
Issue number3
StatePublished - Mar 2009


  • Antibacterial defense
  • Colon ascendens stent peritonitis
  • IL-12
  • Interferon γ IL-10
  • T cells


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