Related Experiment Videos
[Th1/Th2 balance in systemic inflammatory response syndrome (SIRS)]
Hideo Iwasaka1, Takayuki Noguchi
1Anesthesiology, Department of Brain and Nerve Science, Oita University Faculty of Medicine.
Nihon Rinsho. Japanese Journal of Clinical Medicine
|December 16, 2004
Summary
Severe sepsis shifts T-helper (Th) cell activity towards Th2, promoting humoral immunity and potentially causing immune suppression. Modulating this Th2 predominance may offer new sepsis treatments.
Area of Science:
- Immunology
- Cellular Biology
Context:
- Pro-inflammatory cascades following infection, surgery, or trauma can lead to immune dysfunction, sepsis, and organ failure.
- T-helper (Th) cells play a crucial role in the systemic response to infection, with distinct subsets (Th1 and Th2) producing different cytokines that dictate immune responses.
Purpose:
- To investigate the balance between T-helper 1 (Th1) and T-helper 2 (Th2) cell activity in patients with severe sepsis, systemic inflammatory response syndrome (SIRS) without sepsis, and healthy individuals.
Summary:
- Flow cytometry analysis revealed a predominant Th2-mediated immune response in patients with severe sepsis.
- This indicates a polarization of T-helper lymphocyte activity towards the Th2 subset in severe sepsis.
- The observed Th2 shift may contribute to immunosuppression, a common complication in severe sepsis.
Impact:
- Findings suggest that severe sepsis induces a significant shift towards Th2 immune responses.
- This Th2 polarization could underlie the immune dysfunction observed in sepsis.
- Targeting Th cell subset balance presents a potential novel therapeutic strategy for managing severe sepsis.